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Journal of

Infectious Diseases

and Immunity

Volume 4 Number 1 January 2012

ISSN 2141-2375


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Dr. Louis DeTolla

University of Maryland School of Medicine,

10 S. Pine St., MSTF, G-100, Baltimore, MD 21201,


Dr. Wanqiu Hou, PhD

Department of Microbiology-Immunology

Northwestern University Medical School

303 E. Chicago Ave, Chicago, IL 60611


Dr.Murali Gururajan, DVM,PhD

Research Scientist I

Department of Medicine

Cedars-Sinai Medical Center

Los Angeles,


Prof. Wihaskoro Sosroseno

Faculty of Dentistry,

AIMST University, Semeling, 08100 Bedong, Kedah,


Prof. Alan Fenwick

Imperial College, London,

Faculty of Medicine, St Marys W21PG,

United Kingdom.

Dr. Claro N. Mingala

Institution - Philippine Carabao Center,


Editorial Board

Prof. Ludmila Viksna

Riga Stradins University

Linezera str.3, Riga, LV 1006,


Dr. Tommy R. Tong

Montefiore Medical Center of Albert Einstein College of



Dr. Fabrizio Bruschi

universita' di pisa,

school of Medicine,


Dr. Chang-Gu Hyun

Jeju Biodiversity Research Institute(JBRI),

Jeju Hi-Tech Industry Development Institute(HiDI),


Dr. Raul Neghina

Victor Babes University of Medicine and



Dr. Shabaana A. Khader

Children’s Hospital of Pittsburgh,

University of Pittsburgh School of Medicine,

Pittsburgh, PA 15201,


Prof. Fukai Bao

Kunming Medical University,

Kunming, Yunan 650031,


Dr. Liting Song, MD, MSc


Hope Biomedical Research



Dr. Namrata Singh

(ACRP) Association of Clinical Research professional and


courses in Clinical research and Good Clinical practices



Dr. Nuno Cerca

University of Minho,


Dr. Amar Safdar

M. D. Anderson Cancer Center,

1515 Holcombe Blvd, 1460, Houston, Texas 77030,


Dr. Liba Sebastian

Department of Microbiology,

Vijayanagara Institute of Medical Sciences, Bellary,



Dr.Robert W. Tolan, Jr.

Saint Peter’s University Children’s Hospital,

MOB 3110, 254 Easton Avenue, New Brunswick, NJ 08901,


Dr. Nanthakumar Thirunarayanan

National Institutes of Health (NIH),


50 South Dr. Rm 4126,

Bethesda, MD 20850,


Dr. Silonie Sachdeva

Carolena Skin & Laser Center,

1312,Urban Estate, Phase 1 Jalandhar, Punjab-144022,


Dr. Zi-Gang Huang

Institute of Computational Physics and Complex Systems,

School of Physical Science & Technology,

Lanzhou University, Lanzhou 730000,


Dr. Andrew Taylor-Robinson

Institute of Cellular & Molecular Biology,

University of Leeds,

United Kingdom.

Dr. Seth M. Barribeau

ETH Zürich,

Experimental Ecology, Universitätstrasse 16, 8092 Zürich,


Dr. Ikonomopoulos John

Agricultural University of Athens,

Thrasyboulou 44, 15234, Xalandri, Athens,


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Chikere CB, Omoni VT and Chikere BO (2008).

Distribution of potential nosocomial pathogens in a

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Moran GJ, Amii RN, Abrahamian FM, Talan DA (2005).

Methicillinresistant Staphylococcus aureus in

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International Journal of Medicine and Medical Sciences

Journal of Infectious Diseases and Immunity


Table of Contents: Volume 4 Number 1 January 2012


Review on major viral diseases of chickens reported in Ethiopia 1

Hailu Mazengia

Research Article

Detection of IgG, IgA and IgM antibodies against Porphyromonas gingivalis

in gingival crevicular fluid and saliva in patients with chronic periodontitis 10

Marcela Y. Martinez-Guzman, Manuel A. de la Rosa-Ramírez,

Alma Y. Arce-Mendoza and Adrian G. Rosas-Taraco

Journal of Infectious Diseases and Immunity Vol. 4(1), pp. 1-9, 15 January, 2012

Available online at

DOI: 10.5897/JIDIx11.001

ISSN 2141-2375 ©2012 Academic Journals


Review on major viral diseases of chickens reported in


Hailu Mazengia

College of Agriculture and Environmental Sciences, Bahir Dar University, P. O. Box, 79, Bahir Dar, Ethiopia.


Accepted 20 December, 2011

In Ethiopia, the major poultry products come from backyards chickens. But in recent times, more

commercialized poultry farms are flourishing having considerable contribution to the supply of poultry

products, especially to urban areas. There are also attempts to upgrade the productivity of local

chickens through distribution of exotic and cross breeds to the rural areas. These endeavors, however,

are hampered from providing the expected benefits due to various constraints, among which viral

diseases are of greater concern. Some of the viral diseases are thought to be introduced concurrent

with intensification of poultry industry. In addition, the growing numbers of exotic flocks in the

backyard system increases the number of birds which are at risk of getting infected with pathogens in

the environment. The present review article deals with major viral diseases of chickens, their current

status and future challenges to the poultry industry in Ethiopia. Among these, Newcastle disease,

infectious bursal disease and Marek’s disease become serious threats to poultry production. Due to

limited research activities, the epidemiology and the total economic damage caused by this disease are

not fully known. Frequent outbreaks and occurrence of new strains for these viral diseases became a

challenge to the juvenile poultry industry in Ethiopia.

Key words: Chickens, Ethiopia, infectious bursal disease, Marek’s disease, Newcastle disease, viral diseases.


Rural poultry production plays a major role in the

economy particularly of developing countries (Sonaiya,

1990). The larger proportion of rural poultry in the

national flock population of developing countries makes

them worth paying attention to improved management

and breeding. Horst (1989) reported that about 80% of

the poultry population in Africa is kept in backyard

production system. For example, rural poultry constitutes

about 99, 88, 80, and 86% of the national poultry

production of Ethiopia, Uganda, Tanzania, and Nigeria,

respectively (Alamargot, 1987; Kitalyi, 1997). In village

systems, farmers keep poultry for diverse objectives.

They are raised for purposes of hatching, sale, and home

consumption, sacrifices (healing ceremonies) and gifts

(Alemu, 1995). Village chicken products are often the

only source of animal protein for poor households. Eggs

are the source of high quality protein for sick and

malnourished children (Horst, 1989; Kitalyi, 1997). About

20% of the eggs produced from backyard chickens are

eaten or sold (Spradbrow, 1995; Tadelle, 1996). In most

instances after some eggs are retained for hatching, the

household consumes a small proportion but most are

sold to supplement income (Alemu, 1995; Tadelle, 1996).

Meat and eggs are not plentiful in villages and eating

meat is undoubtedly a sign of wealth (Veluw, 1985). This

simply indicates that income generation from village

poultry is more important than consumption for the

farmers (Alemu, 1995).

In Ethiopia, village chickens have been reared for a

long time for similar purposes. They have contributed to

the country’s economy. This is not because they are

productive but are huge in number (Alamargot, 1987).

Constraints which restrict the potential of village chickens

in Ethiopia include; low inputs of feeding, poor

management, the presence of diseases of various

natures and lack of appropriate selection and breeding

practices (Alemu, 1995; Ashenafi, 2000; Tadelle and

Ogle, 2001). In recent years, however, attempts are

underway to enhance poultry productivity and optimize

the contribution of chickens to the national economy.

2 J. Infect. Dis. Immun.

Greater efforts have been made to transform the

production system into a more commercialized and

intensive large-scale system (Ashenafi, 2000). In

addition, exotic breeds and cross-breeds are multiplied in

government owned poultry farms and distributed to

individual farmers via the extension division of the Bureau

of Agriculture and Rural Development to be maintained

and produced under the backyard management system.

This is thought to improve the livelihood and nutrition of

poor farmers and further to contribute to the national

economy at large (Tadelle and Ogle, 2001). Accordingly,

the Bureau of the Amhara Agriculture and Rural

Development (BoARD) schemed poultry development

strategy starting from 2003.

The main purpose of the strategy was to enable

farmers to generate income through rearing day-old

chickens of two breeds Rhode Isle land Red (RIR) and

Lohmann White breeds (LOH) which are hatched and

distributed from poultry multiplication centers located at

Andasa and Kombolcha. However, it is becoming a

growing concern that there is introduction of diseases of

various etiologies into several poultry farms concurrent

with importation of exotic breeds to backyard chickens.

Furthermore, intensification is aggravating the rapid

spread of the prevailing infectious diseases between and

within poultry farms. And the distribution of these exotic

breeds to farmers is creating a great treat to the

indigenous backyard chickens (Alamargot, 1987; Zeleke

et al., 2005a). Among these threats viral diseases like

Newcastle disease (ND), Marek’s Disease and infectious

bursal disease (IBD) are the major health constraints

inflicting heavy losses (Alamargot, 1987; Alemu, 1995;

Ashenafi, 2000; Tadelle and Ogle, 2001; Zeleke et al.,

2005a, b). Therefore, the objectives of this review article


1) To highlight the spread and pathogenesis of major viral

diseases of chickens;

2) To compile the distribution and impact of viral diseases

of chickens reported in Ethiopia;

3) To indicate the direction of research and development

endeavor with regard to the major viral diseases of

chickens in Ethiopia.



Newcastle disease

Newcastle disease (ND) is a highly contagious and the

most dreaded disease of chickens, turkeys and many

other birds (Hanson, 1978; Nonnewitz, 1986; Chuahan

and Roy, 1998; Alexander and Jones, 2001). It is

characterized by the lesions in the respiratory tract,

visceral organs and brain and causes moderate to severe

mortality and morbidity in susceptible flocks. The disease

was first reported for the first time on the island of Java,

Indonesia (Kraneveld, 1926) and Newcastle up on Tyne,

England (Doyle, 1927). It is from this town that the

disease has got its name. According to Spradbrow (1987)

and Alexander (1988) the disease was recognized in

other parts of Asia (Korea, Philippines, India) in the same

and subsequent years. However, several reports exist in

the literature of disease outbreaks, which predated the

year 1926. Hanson (1978) and Alexander (1988)

reviewing the literature, stated that ND first occurred in

and around sea ports, apparently as a result of

commercial activities by sea, and then spread to the

interior of the countries much later.

Newcastle disease (ND) is caused by a group of

closely related viruses that form the avian Paramyxovirus

type 1 (APMV-1) serotype. Some serological

relationships have been demonstrated between

Newcastle disease virus (NDV) and other Paramyxovirus

serotypes, the most significant being that with viruses of

APMV-3 serotype. For many years NDV strains and

isolates were considered to form a serologically

homogenous group and this has been the basis of

vaccination procedures employed for prophylaxis in most

countries (Al-Garib, 2003). However, more specific

serological techniques most notably monoclonal antibody

based serology, have shown the existence of

considerable antigenic variation between the different

strains of NDV. Based on the disease produced in

chickens under laboratory conditions, NDVs have been

placed into five pathotypes; viscerotropic velogenic NDVs

(VVND) cause a highly severe form of the disease in

which hemorrhagic lesions are characteristically present

in the intestinal tract, neurotropic velogenic NDVs cause

high mortality following respiratory and nervous signs,

mesogenic NDVs cause respiratory and sometimes

nervous signs with low mortality, lentogenic respiratory

NDVs cause mild or inapparent respiratory infection and

asymptomatic enteric NDVs cause inapparent enteric

infection (Chuahan and Roy, 1998; Alexander and Jones,

2001). Approximately from 800 known avian species,

only about 236 species have a record of NDV isolation.

The disease is seen most frequently in domestic poultry,

including guinea fowl, a species more susceptible than

turkey and peafowl (Allan et al., 1973). Ducks, geese,

partridge, and quill are relatively resistant (Higgins, 1971;

Allan et al., 1973). The most resistant species appear to

be aquatic birds, while the most susceptible are

gregarious birds forming temporary or permanent flocks

(Kaleta and Baldauf, 1988).

Spradbrow (1988), reviewing the 1985 animal health

yearbook of the Food and Agriculture Organization of the

United Nations (FAO), summarized that lentogenic or

mesogenic strains of NDV were present in most countries

of Asia, Africa, and Europe, and in the USSR. More than

one third of the countries of Asia and one fifth of the

countries of the world acknowledged the presence of the

velogenic strains of the virus. In contrast, the countries of

Oceania were relatively free of NDV. Some countries

ecognized the presence of the avirulent strains of the

virus, while many of the island states were apparently

free from all pathtypes of NDV. A sequence of events

following introduction of NDV into chickens is initiated by

multiplication of the virus at the site of introduction.

Initially the virus replicates in the mucosal epithelium of

the upper respiratory and intestinal tracts. Then follows

release of the virus into the bloodstream, a second cycle

of multiplication occurs in visceral organs producing a

secondary viremia. This leads to infection of other target

organs such as lungs, intestine and central nervous

system (Murphy et al., 1999). Signs of the disease and

liberation of the virus into the environment are associated

with the second release of the virus into the bloodstream.

An exception occurs with large airborne exposures where

the virus replicates in and is disseminated from the

epithelium of the respiratory tract (Beard and Hanson,


Pathologic changes associated with ND vary greatly

from bird to bird, flock to flock and from one geographic

region to another. Gross lesions vary depending on virus

and may also be absent. Cadavers of birds that died

because of virulent NDV, usually have a dehydrated

appearance. These lesions are often particularly

prominent in the proventriculus, small intestine and ceca.

These organs are markedly hemorrhagic which

apparently results from necrosis of the intestinal wall or

lymphoid tissues, such as cecal tonsils (Chuhhan and

Roy, 1998; Alexander and Jones, 2001). Little evidence

of gross lesions is found in the central nervous system

even in birds showing neurological signs prior to death.

Gross pathological lesions are usually present in the

respiratory tract in birds with respiratory illness. They

consist predominantly of hemorrhagic lesion and

congestion of the trachea and in addition air sacculitis

may be evident. Egg peritonitis is often seen in laying

hens affected with virulent NDV (Beard and Hanson,

1984; Murphy et al., 1999). Histopathologically,

hyperemia, edema, hemorrhage, and other changes in

blood vessels are found in various organs. In general, in

most tissues and organs involved, the lesions include

hyperemia, necrosis, cellular infiltration, and edema.

Lesions in the central nervous system are characterized

by nonpurulent encephalomyelitis (Beared and Hanson,

1984; Al-Garib, 2003). For virus isolation in the head,

spleen and long bones from acutely sick birds should be

collected after disinfection in flame. The brain, bone

marrow and spleen tissues are crushed into pieces using

pestle and mortar with 5 mL broth, 2000 I.U. of penicillin

and 5 mg of streptomycin. In addition to virus isolation

other tests conducted to confirm the disease include:

hemagglutination test, hemagglutination inhibition (HI)

test, virus neutralization test, fluorescent antibody

technique (FAT) and complement fixation test (CFT)

(Chuahan and Roy, 1998).

Effective control of Newcastle disease requires good

sanitation, management, quarantine, an appropriate

Mazengia 3

vaccination program, and monitoring system, including

serotyping and pathogenicity testing of isolated virus

(Meulemans, 1988). According to Hanson (1978) a

minimum of 70% of flocks in high risk areas must be

included in sanitary and combined vaccination programs

if control is to be effective. Vaccination against ND can be

performed using either live or inactivated vaccines

(Meulemans, 1988).The effectiveness of ND vaccines in

the control of the disease, whether under closed

commercial, semi-closed intensive, or under free range

rural systems in tropical countries, depends on the

virulence of the field strain, immunological state of the

birds and the method of vaccine application (Meulemans,


The results of vaccine trials in Ethiopia showed that

conventional (HB1 and La Sota) and the thermostable

NDV-I2 vaccines give similar antibody response and

protection against challenge when given via the ocular

and the drinking water route. The oral application of NDV-

I2 was also shown to be effective with barley as vaccine

carrier, if barley was pre treated by parboiling (Nasser,


Infectious bursal disease

Infectious bursal disease (IBD) is a highly contagious

immunosuppressive infection of immature chickens

caused by a double stranded RNA virus in the genus

Avibirnavirus (Faragher, 1972; Dobos et al., 1979; Muller

et al., 1979; Lukert and Saif, 1997). Infectious bursal

disease also known as Gumboro disease was first

recognized by Cosgrove (1962) as a clinical entity, in

1957 in USA. Allan et al. (1973) reported that IBD virus

(IBDV) infections at an early age were

immunosuppressive. The existence of a second serotype

was reported in 1980 (McFerran et al., 1980). Control of

IBD viral infection has been complicated by the

recognition of “variant” strains of serotype 1 IBDV that

were found in the Delmarva poultry producing areas in

the US (Rosenberger et al., 1985). Infectious bursal

disease (IBD) also known as Gumboro disease is caused

by infectious bursal disease virus (IBDV) that belongs to

the genus Avibirnavirus of the family Birnaviridae.

Two serotypes of the virus are recognized and

designated as serotype 1 and 2. Only serotype 1 appears

to be pathogenic to chickens (Murphy et al., 1999).

Antigenic and pathogenic variant strains have been

documented. The range in virulence of strains in serotype

1 varies from mild to intermediate to intermediate plus.

Very virulent strains of IBDV also exist (Chuahan and

Roy, 1998). One of the most interesting features of IBDV

is its ability to remain infectious for a very long period of

time and its resistance to commonly used disinfectants.

Infectious bursal disease is usually a disease of three to

six week old chickens. But an early subclinical infection

before three weeks of age was also observed (Lukert and

4 J. Infect. Dis. Immun.

Saif, 1997). All breeds are affected but severe reactions

with highest mortality rate were observed in White

Leghorn (Lukert and Saif, 1997). Chowdhury et al. (1982)

observed higher mortality rate (70 to 80%) in Fayoumi

breed as compared to that in White Leghorn (40%) during

field outbreaks. There is no report of egg transmission of

IBDV. Infected birds excrete virus in their dropping at

least for 14 days (Baxendale, 2002). Chickens are the

only known avian species to develop clinical disease and

distinct lesions when exposed to IBDV (Lukert and Saif,

1997). The most common mode of infection is through

the oral route. Conjuctival and respiratory routes may

also be involved (Sharma et al., 2000). Following oral

infections, the virus replicate in gut associated

macrophages and lymphoid cells. From there, the virus

enters the portal circulation leading to primary viremia.

Within 11 h of infection, viral antigen can be detected in

bursal lymphoid cells. Large amount of the virus released

from the bursa produce a secondary viremia, resulting in

localization in other tissues. IBDV causes severe immune

suppression in young chickens by its lymphocytolytic

effects on surface IgM bearing B-cells.

Furthermore, immune suppression may be associated

with the effect of the virus on T-cells and macrophages

(Lukert and Saif, 1997; Murphy et al., 1999). Infectious

bursal disease virus replication in target organ mainly in

the bursa of Fabricius leads to extensive lymphoid cell

destruction in bursal follicles. Early in the infection

process, the bursa becomes edematous, hyperemic and

creamy in color with prominent longitudinal striations.

Later on, lymphoid follicles of the bursa become totally

necrotic and in surviving birds the follicles will be devoid

of lymphoid cells (Chuahan and Roy, 1998; Baxendale,

2002). Highly virulent virus strains could also cause

depletion of lymphoid cells in the thymus, spleen and

bone marrow. Depletion of B-cells from the medullary

areas results in cystic cavities that are obvious under light

microscopy. In long standing cases, there is an increased

connective tissue mass in the interfolicular areas

replacing the depleted lymphoid tissues (Sharma et al.,

2000; Negash, 2004). Classical IBD is characterized by

acute onset, relatively high morbidity and low flock

mortality in 3 to 6 week old-broilers or replacement

pullets. Diagnostic lesions include muscle hemorrhages

and bursal enlargement (Hanson, 1978; Chuahan and

Roy, 1998; Baxendale, 2002). The dramatic impact of a

very virulent IBD virus can be reduced by biosecurity

methods that are cleaning and disinfection, since the

virus is very stable for months.

It is largely excreted through feces hence contaminated

litter, feed and water have to be burnt or buried deep

under the lime cover. Besides this other measures are;

lower stocking densities, increasing intervals between

flocks and complete removal of organic waste between


In areas where management practices to reduce virus

concentration are used, the disease trends to occur at a

later age, and immunosuppressive form of infection is

reduced (Stwart-Brown and Grieve, 1992). Administration

of inactivated vaccines to breeder hens induces longstanding

and high levels of antibodies in the hatched

chicks. But in some areas where very virulent IBD virus

has caused significant losses the producers do not adopt

inactivated vaccination. But intensive live virus

vaccination program is used in the hatched chicks from

the unvaccinated breeder hens. Such chicks escape the

strong risk of immunosuppressive form of the disease

(Chuahan and Roy, 1998).

Marek’s disease

The causative agent for Marek’s disease (MD) is a cell

associated lymphotropic herpesvirus. Due to its

lymphotrpic nature, MD virus (MDV) was originally

classified in the family Herpes viridae as a member of

subfamily Gammaherpesvirinae (Chuahan and Roy,

1998). However, on the basis of genomic organization,

MDV is currently classified with the viruses of subfamily

Alphaherpesvirnae. Three serotypes of MDV and related

Herpes viruses have been defined. Serotype 1 includes

all the pathogenic or oncogenic strains of these viruses.

Serotype 2 includes naturally non-attenuated strains of

MDV. Serotype 3 includes turkey herpesvirus (HVT), the

non-oncogenic MDV related virus isolated from turkey.

New pathtypes have been emerging indicating

continuous evolution of MDV towards greater virulence

(Venugopal et al., 2001). The pathogenesis of MD is

complex, with infection occurring throughout the

respiratory route from inhalation of poultry house dust

contaminated with the virus. After an early cytolytic

infection mainly of the B-lymphocytes in the bursa, spleen

and thymus, at 3 to 5 days post infection, the virus infects

activated T-lymphocytes, mainly of the CD4 + phenotypes.

The infection in the T-lymphocytes becomes latent at 6 to

7 days post infection and the virus is spread throughout

the body by the infected lymphocytes that persist as a

cell-associated viremia. A secondary cytolytic infection

occur in the feather follicle epithelium form about ten

days after infection, from where infectious cell-free virus

is produced and shed into the environment in feather

debris and dander. The lately infected T- lymphocytes are

subsequently transformed leading to the development of

lymphomatous lesions in visceral organs. The main target

cells for transformation in natural infections are CD4 + Tcells,

although the virus also has the potential to

transform CD8 + T-cells (Murphy et al., 1999; Venugopal

et al., 2001).

The characteristic gross lesions in the classical form of

MD are the enlargement of one or more peripheral

nerves. The most commonly affected nerves that are

easily seen on post mortem examination are the bracial

and sciatic plexus and nerve trucks, celiac plexus,

abdominal vagus and intercostals nerves. The affected

nerves are grossly enlarged, and often are three or four

times their normal thickness (Chuahan and Roy, 1998.

The normal cross-striated and glistering appearance of

the nerves is lost; they have grayish or yellowish

appearance and are edematous. Lymphomas are present

in some chronic form of the disease most frequently as

small, soft, grey, tumors in the ovary, kidney, heart, liver

and other tissues. In the acute form, the typical lesion is

widespread, diffuse lymphomatous involvement of

visceral organs such as liver, spleen, ovary, kidney, heart

and proventriculus. Sometimes lymphomas are also seen

in the skin around the feather follicles and in the skeletal

muscle. The liver enlargement in young birds is usually

moderate compared to the adult birds. In acute cytolytic

form of the disease caused by some virulent isolates, the

thymus and buras of Fabricius may disappear completely

due to extensive atrophic changes. The peripheral nerves

in both classical and acute form of the disease are

affected by proliferative inflammatory or minor infiltrative

changes (Murphy et al., 1999; Venugopal et al., 2001).

The clinical signs, combined with post-mortem findings,

will confirm the diagnosis of Marek’ disease in most

cases, and, most importantly, rule-out other diseases.

Enlargement of nerves such as the sciatic nerve are

commonly seen at post-mortem. Changes in one or more

internal organs may also be observed (Chuahan and

Roy, 1998; Venugopal et al., 2001).

Although vaccines are commonly used in the

commercial poultry industry, small numbers of doses

cannot be purchased for use in backyard flocks. For

backyard flocks, the best protection against Marek’s

disease is obtained by buying, from a commercial source,

birds that have been correctly vaccinated. Vaccination

alone will not prevent Marek's disease. Particularly for

commercial flocks, it is important to have good

biosecurity to ensure that vaccinated chicks will develop

immunity before they are subjected to a severe challenge

of virus. For example, chicks need to be reared

separately so that they are free from the infected fluff and

dust of older birds. Standard hygiene measures are also

important, including a thorough clean-out and disinfection

of sheds and equipment between batches of chicks with

a disinfectant effective against viruses. Good nutrition

and maintenance of freedom from other diseases and

parasites are also very important. These practices will

help maintain the flock’s health and to ensure that the

birds have optimum resistance against Marek’s disease

infection (Murphy et al., 1999; Venugopal et al., 2001).



Research and case reports coming from various regions

of the country indicated that viral diseases are posing a

growing threat to the young poultry industry flourishing in

the country. In addition, the intensification and

Mazengia 5

dissemination of exotic breeds to villages has created

chicken population, which is susceptible to the major viral

diseases. The loss due to viral diseases like Newcastle

disease and infectious bursal disease is escalating in

recent years. Some farmers have even given up rearing

poultry because of increasing disease problems

(Edwards, 1992; Tadelle, 1996; Ashenafi, 2000; Zeleke et

al., 2005a). Newcastle disease is mentioned as the major

disease problem in commercial poultry farms and village

chickens in most parts of the country. The disease has

many different local names in different areas and the

most common one is “Fengele’’ (Edwards, 1992; Tadelle,

1996; Nasser, 1998; Ashenafi, 2000; Halima et al., 2007),

which means sudden dorsal prostration and signifies the

acuteness and severity of the disease. In 1995, an

outbreak of ND in the surrounding areas of Debre Zeit,

Nazareth and Addis Ababa killed almost 50% of the

local/indigenous chickens (Nasser, 1998) (Table 1). A

serological survey conducted in six villages from central

Ethiopia (non-vaccinated birds) revealed a high

prevalence (43.68%) of NDV antibodies (Ashenafi, 2000).

Another study conducted in village chickens in the

southern and rift valley districts of Ethiopia indicated that

ND is endemic in the area. Higher seroprevalence rates

(22.51%) of NDV antibodies were verified in all the dry

areas of the rift valley and a prevalence of 14.13% was

reported in some parts of the wet southern districts

(Zeleke et al., 2005a) (Table1).

In Ethiopia, outbreaks of ND usually happen at the

beginning of the main rainy season (end of May and

beginning of June). Nevertheless, this seasonal pattern

seems to have changed after the 1984 to 1986

villagenization programs were launched, and it has

become a problem throughout the year, although it is still

more serious at the beginning of the main rainy season

(Tadelle and Jobre, 2004). Nasser (1998) has also

reported the occurrence of the disease all year round.

Ashenafi (2000), on the other hand, reported that few

clinical cases of ND during the dryer months of the year

even if the seroprevalence of antibodies against NDV

remained high throughout the year like reports by other

studies (Tadelle and Jobre, 2004). It is possible to say

that currently there are no low risk areas for ND

remaining in Ethiopia. The disease has already become

endemic in village poultry population and thus it recurs

every year inflicting heavy losses (Tadelle and Jobre,

2004). It has been indicated that velogenic strains of NDV

are widely distributed throughout the country (Nasser,

1998). But in general the epidemiology of ND in the

village poultry in Ethiopia is poorly understood and there

is no appropriate investigation and control strategy

designed against the disease. This is due to lack of

disease monitoring capacity in the Veterinary Services

Department of the Ministry of Agriculture and Rural

Development (Tadelle and Jobre, 2004).

Farmers start to consider, therefore, losses due to

diseases as normal and natural (Tadelle, 1996; Nasser,

6 J. Infect. Dis. Immun.

Table 1. Summary of occurrences of Newcastle disease infectious bursal disease and Marek’s disease in certain areas in Ethiopia.

Disease Location Period/year







rates (%)


Incidence (%) References

Central highlands of Ethiopia (Dembi, Shola and Lemlem poultry farms) 1983-1995 14.90 58.50 Nasser, 1998

State poultry farms of Ethiopia 1983-1995 2.3 - Nasser, 1998

Central high lands of Ethiopia 1999-2000 43.7 - Ashenafi, 2000

Rift valley 2004-2005 22.51 - Zeleke et al., 2005a

Wet highland districts 2004-2005 14.13 - “ “

Bahir Dar District October 2007-April 2008 - 29.60 Mazengia et al., 2010

Farta District October 2007-April 2008 - 21.70 “ “

Debre Zeit overall (mortality) 2004-2005 49.89 - Zeleke et al., 2005b

Layer (morality) 2004-2005 25.08 - “ “

Broiler (mortality) 2004-2005 56.09 - “ “

Debre Zeit (seroprevalence) 2004-2005 - 93.30 “ “

Andasa poultry farm (young mortality) Oct-Nov 2006 72 - Woldemariam and Wossene, 2007

Andasa poultry farm (adult mortality) Oct-Nov 2006 7 - “ “

Andasa poultry farm (seroprevalence) Oct-Nov 2006 - 100 “ “

Bahir Dar October 2007-April 2008 38.9 29.40 Mazengia et al., 2009, 2010

Farta October 2007-April 2008 17.40 21.70 “ “

1998) and they fail to report outbreaks to the

veterinary authorities. Infectious bursal disease is

another newly emerging disease of chickens in

Ethiopia. This disease has been speculated to be

introduced concurrent with the increased number

of commercial poultry farms flourishing in the

country (Zeleke et al., 2002; Woldemariam and

Wossene, 2007). The report of introduction of IBD

in the country has come only recently where

chickens with clinical signs and lesions of IBD

have been shown to be positive for anti-IBDV

antibody (Zeleke et al., 2005b) (Table 1). Report

of IBD outbreak in Debre Zeit in 20 to 45 days old

broiler and layer chickens indicated that the

mortality rate of the disease in different poultry

houses ranges from 45-50%. The overall mortality

however was 49.89%. Broiler mortality due to IBD

was 56.09%, while 25.08% for layer chickens and

the seroprevalence of IBDV antibody was 93.30%

(Zeleke et al., 2005b) (Table 1). Case report from

Andasa poultry farm, northwest Ethiopia, indicated

that the overall mortality of birds due to IBD was

72% in young (1 to 70 days of age) and 7% in

adults (> 70 days old), showing young birds are

more susceptible than adults. In this study a 100%

seroprevalence has been shown in the study

population (Woldemariam and Wossene, 2007).

These reports indicate that the disease is present

in many parts of the country and is disseminating

at a faster rate in recent years. Despite the fact

that IBD incidences are increasing at alarming

rate all over the country where commercial poultry

production is intensified and even in the backyard

chickens, there is not any endeavor towards the

implementation of cost effective control strategies

of IBD. But there is recommendation from the

Federal Ministry of Agriculture and Rural

Development that regional states should

implement vaccination against IBD to combat the

loss of poultry at this stage (Mazengia 2010).

Future challenges and prospects regarding

the control of major viral diseases of chickens

in Ethiopia

Among the different food sources, poultry

products contribute significantly to the country’s

food demand. With the increasing population of

the country, there is an increasing demand for the

supply of food. Under the prevailing management

situations, it may be difficult to fulfill these demands in a

short time. Therefore, intensification and upgrading of the

potential of birds will be inevitable to provide surplus

products (Hailemariam et al., 2006). In line with this aim

different chicken strains have been introduced into this

country. The chicken strains imported are temperate

breeds that are less adapted to the heat stress and

disease challenges in the country. Accompanying with

the intensification of poultry farming, there are

occurrences of epidemics of newly introduced diseases

and/or epidemics of endemic diseases like ND and IBD

(Zeleke et al., 2005a, b). These diseases have incurred

considerable economic loss to the country. At present,

the most important challenge at the door is the failure of

early diagnosis and reporting of the different poultry

diseases when they occur and this has hindered the

success of control mechanisms implemented in some

parts of the country (Tadelle and Jobre, 2004).

Absence of research-based investigation approaches

resulted in lack of knowledge of the prevalent strain of

viruses and information on the overall epidemiological

patterns of the different viral diseases. This has been

posing a challenge especially for the success of vaccines

used at these times (Wit and Baxendale, 2004). In

diseases like MD, even if successful vaccination

programs have been implemented, it remained an

economically important disease basically because of the

combined effect of relatively high vaccination costs, a

continued evaluation of the virus to a more virulent strain

and the early challenge by MDV before vaccine-induced

protection (Schat, 2004). Lack of integrated approaches

for the control of predisposing diseases has led to the

ineffectiveness of vaccination programs. A good example

is failure of ND vaccination in areas where there is no

integrated approach for the control of IBD (Wit and

Baxendale, 2004; Woldemariam and Wossene, 2007).

On top of this, most control strategies designed in the

country do not take into consideration the local chickens,

and this may lead into the failure of most strategies

(Tadelle, 1996; Tadelle and Ogle, 2001; Hailemariam et

al., 2006). In Ethiopia, lack of coordinated implementation

of importation policy and quarantine services have

opened the door to the introduction of many poultry

diseases that have not been reported previously like IBD.

Birds are imported without health certificates and are not

declared whether they were vaccinated against major

viral diseases of chicken or not (Zeleke et al., 2005a, b).

Another challenge in the protection of chickens against

major pathogens is that chickens are challenged with the

viruses, as well as other pathogens, as soon as they are

placed on the farms, which is in general within 1 to 3

days after hatching. This will be before the time of

vaccine-induced protection even if we vaccinate day old

chicks (Sharma and Burmester, 1982). Thus, this directs

the vaccination of embryos 3 days before hatching. In

Ethiopia, lack of coordinated implementation of

importation policy and quarantine service has opened the

Mazengia 7

door to the introduction of many poultry disease that have

not been reported previously like IBD. Birds are imported

without health certificate and are not declared whether

they were vaccinated against major viral diseases of

chicken or not (Chuan and Roy, 1998; Baxendale, 2002).

In the future, there is a tendency of growing poultry

industry and there are some promising research outputs

that could help effective control of viral diseases

threatening this sub-sector. Production of safe and

effective vaccines are underway to minimize the effects

of these agents. In recent times, an immune complex

(ICX) vaccine against IBD is prepared.

In addition to improved safety, the ICX vaccine is

known to induce early immunity when administered to

embryos as evidenced by higher antibody titers or higher

levels of protection. Antigens preserved in the form of

ICX are believed to maintain humoral immune responses

for a long duration (Tew et al., 1980; Jerurissen et al.,

1998) and ICX vaccines are also believed to be

insensitive to maternal antibody and thus can also be

administrated to day-old chicks irrespective of the level of

maternal antibody (Jerurissen et al., 1998). The research

of Sharma and Burmster (1982) has brought the idea of

in ovo vaccination into the vaccine technology. In ovo

vaccination or embryo vaccination is the administration of

vaccines into fertile chicken embryos at incubation day 18

to 19 after drilling a hole via the eggshell. The embryos

may ingest the surrounding amnion with the vaccine and

thus the antigen can stimulate the immune competent

cells of gut-associated lymphoid tissues. This is known to

induce the development of an earlier and a more solid

protective immunity. It is also plausible that the highly

efficient administration of the in ovo vaccine reduces the

percentage of chicks that are not properly vaccinated,

thus reducing the number of chicks at risk. Currently, in

ovo administered vaccines are available for ND and IBD

(Jerurissen et al., 1998).


Newcastle disease, infectious bursal disease and

Marek’s disease are among major viral diseases of

chickens in Ethiopia. They are highly contagious serious

threats of the poultry industry. Although, these diseases

are introduced recently to the country, they cause

significant losses to both commercial poultry farms as

well as rural poultry production. Although there are some

studies that indicated poultry diseases of viral origin

became endemic throughout the country, information on

the epidemiology and as well as the occurrence of new

strains of these diseases s scanty. The following points

are recommended as they are important to design

strategies to control and prevent these diseases:

1) In depth studies should be done on investigation of the

epidemiology of these viral diseases;

8 J. Infect. Dis. Immun.

2) Knowledge on the use of vaccines against this disease

should be exploited, so as to have cost effective

prevention methods; and

3) Attempts should emphasize on the identification of

local viral strains to design cost effective vaccine.


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Journal of Infectious Diseases and Immunity Vol. 4(1), pp. 10-15, 15 January, 2012

Available online at

DOI: 10.5897/JIDI11.023

ISSN 2141-2375 ©2012 Academic Journals

Full Length Research Paper

Detection of IgG, IgA and IgM antibodies against

Porphyromonas gingivalis in gingival crevicular fluid

and saliva in patients with chronic periodontitis

Marcela Y. Martinez-Guzman 1 , Manuel A. de la Rosa-Ramírez 1 , Alma Y. Arce-Mendoza 2 * and

Adrian G. Rosas-Taraco 2

1 Facultad de Odontología, Periodontics and Faculty of Medicine and University Hospital, Universidad Autonoma de

Nuevo Leon, Monterrey, Nuevo Leon, Mexico.

2 Department of Immunology, Faculty of Medicine and University Hospital, Universidad Autonoma de Nuevo Leon,

Monterrey, Nuevo Leon, Mexico.

Accepted 21 November, 2011

Humoral immune response is an important host mechanism against periodontopathogenic

microorganisms, such as Porphyromonas gingivalis. P. gingivalis is the most frequent causative agent

of chronic periodontitis in Mexico, but its detection presents difficulties. The aim of this study was to

identify antibodies against semi-purified culture-secreted proteins of P. gingivalis in saliva and gingival

crevicular fluid of patients with chronic periodontitis. Semi-purified culture-secreted proteins of P.

gingivalis were immobilized in Enzyme-Linked Immunosorbent Assay (ELISA) plaque to detect IgA, IgG

and IgM antibodies in saliva and gingival crevicular fluid from chronic periodontitis patients. IgG

antibody against proteins from P. gingivalis was detected in 65% of the samples of patients, 27% of

patients had IgA antibodies, while IgM was detected in 45% of patients. IgG, IgA and IgM antibodies

were detected in saliva and gingival crevicular fluid mainly in patients with severe chronic periodontitis,

confirming that P. gingivalis could be the causative agent of the infection.

Key words: Antibodies, gingival crevicular fluid, Porphyromonas gingivalis, and saliva.


Chronic periodontitis induces a chronic inflammatory

response of the periodontium to bacterial plaque(Haffajee

and Socransky 2000). Inflammation may lead to

destruction of the tooth-supporting tissues and eventually

possible tooth loss. Specific microorganisms or groups of

microorganisms have been related to different forms of

periodontitis. Porphyromonas gingivalis is a Gramnegative

and anaerobic bacterium and it is considered to

be a major periodontopathogen in chronic periodontitis

(World Workshop in Periodontics, 1996; Haffajee and

Socransky, 2000, 2005; Socransky et al., 1998). During

chronic periodontitis both cellular and humoral immune

responses are activated for infection control (Haffajee

*Corresponding author. E-mail: or Tel: +52(81)83294211. Fax:


and Socransky, 2000, 2005). The role of humoral

immunity in chronic periodontitis has not been clarified,

though a protective role has been demonstrated (Kinane

et al., 2011; Kinane and Lappin, 2002). The rate of

periodontal tissue breakdown has been associated with

host susceptibility to periodontitis. Moreover, host

predisposition to disease may relate to innate host

defence and the subsequent activation of adaptative

immune response (Deo and Bhongade. 2010).

The relationship between specific IgA, IgG and IgM

antibodies against P. gingivalis and periodontal diseases

is a controversial issue. High IgG antibody levels against

P. gingivalis have been detected in adults with severe

periodontitis, compared with healthy individuals (Mouton

et al., 1981; Suzuki et al., 1984; Vincent et al., 1985;

Califano et al., 1997; Ebersole, 1990). However, certain

investigators have reported a significant decrease in

specific IgG immunoglobulins in deep periodontal pockets

(>4 mm) and therefore support the concept that humoral

immune response is not protective (Kinane et al., 1993;

Mooney and Kinane, 1997). Another study did not detect

a significant increase in serum antibodies levels to P.

gingivalis (Haffajee et al., 1995). It has been proved that

antigenic components produced by P. gingivalis could

induce host immune response. P. gingivalis antigens,

such as arginine-specific gingipains (RgpA, RgpB) and

lysine-specific gingipain (Kgp) have been demonstrated

to induce a significant humoral response (Nakagawa et

al., 2003). RgpA and Kgp are able to induce the

production of high titers of IgG antibody in immunized

rabbits (Nakagawa et al., 2001). Moreover, another study

revealed that serum of generalized aggressive

periodontitis patients had elevated levels of IgG anti-P.

gingivalis and gingipain antibodies (Gibson et al., 2005).

The aim of the present study was to determine the levels

of IgM, IgG and IgA antibodies in gingival crevicular fluid

or saliva of subjects with severe chronic periodontitis, in

comparison with periodontally healthy subjects.


Study population

The population of the study was divided into an experimental group,

including 29 chronic periodontitis patients (15 females and 14

males), aged 30 to 68 years (mean age, 46.3±7.5 years) and a

control group, comprising 10 periodontally healthy subjects (8

females and 2 males), aged 30 to 62 years (mean age, 46.5±10.5

years). Study participants were derived from the Department of

Periodontics, Facultad de Odontologia, Universidad Autonoma de

Nuevo Leon, Monterrey, Mexico. The study protocol was approved

by the Bioethics Committee at the Universidad Autónoma de Nuevo

Leon and approved this project according to the International

Review Board regulations. Informed consent was obtained from

each patient. Selection criteria for patient inclusion in the

experimental group were:

1) Patients with moderate to severe chronic periodontitis;

2) Systemically healthy;

3) Not having received antibiotic medication within the preceding

three months;

4) Not having received periodontal therapy in the preceding six


5) Non-smokers; and

6) Non-pregnant women.

In the control group, the inclusion criteria were the same, except for

criterion 1, where subjects should be periodontally healthy.

Screening periodontal examination

The following clinical periodontal parameters were recorded for

each subject: plaque index (Nakagawa et al., 2003), gingival index

(Nakagawa et al., 2001), probing depth and clinical attachment

level. Plaque was measured mesio-facial and disto-facial. Probing

depth was registered with a North Caroline probe. The probing

force applied was standardized and all clinical parameters were

performed by a single investigator. The aforementioned indexes,

as well as mean plaque and gingival index were used as diagnosis

criteria for periodontal disease rather than clinical criteria.

Sample collection

Martinez-Guzman et al. 11

Gingival crevicular fluid (GCF) samples were collected in the

experimental and control groups. The collection of gingival

crevicular fluid was performed, using standard methods previously

described in the literature (Löe and Holm-Pedersen, 1965;

Daneshmand and Wade, 1976; Hancock et al., 1979). Before GCF

samples were collected, the tooth selected for sampling was

cleaned of supragingival plaque, dried with gauze to remove saliva

and isolated with cotton rolls placed in the mucobuccal fold.

Subsequently, one filter strip (Periopaper strips) was gently placed

at the entrance of the gingival crevice of the tooth avoiding blood

inclusion. The filter strips were subsequently removed, placed in

microtubes and stored at -20°C until used. Six samples were

randomly collected from each subject. The unstimulated saliva from

the floor of the mouth was collected directly into microtubes with

sterile Pasteur pipettes (Avitrolab, China). A volume of 1 ml of

saliva was collected from each subject and stored at -20°C until


P. gingivalis culture

P. gingivalis (Pg) ATCC 33277 was grown on blood agar plates for

5 to 6 days in an anaerobic chamber with Gas Pack System (BD,

Franklin Lakes, NJ USA) in an atmosphere containing 80% N2, 10%

H2 and 10% CO2. subsequently, P. gingivalis ATCC 33277

(Manassas, VA, USA) was inoculated on thioglycolate medium and

after 48 h incubation, the culture secreted protein of the bacteria

was obtained by centrifugation at 10,000 x g for 15 min at 4°C and

the cellular pellet was sonicated to obtain the protein of cellular


Semi-purified culture-secreted proteins from P. gingivalis

Proteins were obtained by precipitation using 50% ammonium

sulfate (v/v) at 4°C. The precipitate was resuspended in distilled

water and dialyzed against distilled water until absence of salts was

observed. Protein concentration was determined by the Bradford

method (Gibson et al., 2005), and proteins were lyophilized and

then sterilized by filtration through a 0.2 µm-pore size filter

(Millipore, Billerica, MA, USA) and stored at -20°C until its use.

Cell extracts from P. gingivalis

The bacterial cell pellet was washed in phosphate-buffered saline

(PBS) with a concentration of 0.1 M and pH=7, and resuspended in

sterile saline solution to an optical density of 1.0 at a wavelength of

690 nm (model 750 spectrophotometer; Beckman, Brea CA, USA).

The bacterial suspensions were sonicated using a Branson Sonifier

450 (Branson, Danbury, Connecticut, USA). The insoluble debris

was removed by centrifugation at 10,000 x g for 30 min at 4°C. The

protein concentration was determined by the Bradford method

(Gibson et al., 2005), lyophilized, sterilized by filtration through a

0.2 µm-pore size filter (Millipore, Billerica, MA, USA) and stored at -

20°C until its use.

IgA, IgM and IgG antibodies detection in saliva and gingival

crevicular fluid by enzyme-linked immunosorbent assay


Culture-secreted proteins (0.01 µg/well in 200 µl acetate buffer with

pH=5) and cell extract (0.05 µg/well in 200 µl PBS with pH=7.4)

from Pg ATCC 33277 were immobilized on 96-well polystyrene

plates overnight at 4°C. Five washes using PBS with a

12 J. Infect. Dis. Immun.

IgM detection (OD 492 nm)

IgM detection (OD 492 nm)

A .10




.5 B 0.5

IgM detection (O.D. 492 nm)

0.08 .08


0.07 .07







0.04 .04



0.02 .02




0.00 IgG


0 0.0



.6 .8 1.0 1.2 1.4 1.6 1.8 2.0 2.2 2.4

.7 Patients .9 1.1 1.3 1.5 1.7 Control 1.9 2.1 2.3 2.5



.6 .8 1.0 1.2 1.4 1.6 1.8 2.0 2.2 2.4

.7 Patients .9 1.1 1.3 1.5 1.7 Control 1.9 2.1 2.3

IgA detection (OD 492 nm)




IgA detection (O.D. 492 nm)



0.2 .2



IgG detection (O.D. 492 nm)



0.3 .3



0.1 .1





.6 .8 1.0 1.2 1.4 1.6 1.8 2.0 2.2 2.4


.9 1.1 1.3 1.5 1.7 Control

1.9 2.1 2.3 2.5

Figure 1. Antibodies in gingival crevicular fluid of chronic periodontitis patients, compared with periodontally healthy

subjects. Presence of antibodies against semi-purified culture filter antigens from Porphyromanus gingivalis A) Ten

patients with chronic periodontitis shown IgM levels up of control; b) 8 patients had IgG antibodies and c) 8 patients

had IgA antibodies against semi-purified culture filter antigens.

concentration of 0.1 M and pH=7.2 were performed and 5% skim

milk (BD Difco TM , Sparks MD, USA) dissolved in PBS was used to

block unspecific binding by incubation at 37°C for 1.5 h. Saliva (for

IgA detection) and gingival crevicular fluid (for IgM and IgG

detection) obtained from patients and healthy controls were added

on the plate and incubated for 1 h at room temperature, using

shaking to 300 rpm. Three washes were performed using washing

solution, PBS with a concentration of 0.1 M and pH=7.2, and a

0.05% Tween 20, (Sigma Aldrich, St. Louis, Mo, USA).

Bound antibodies were visualized using horseradish peroxidasecoupled

goat anti-human IgG (γ-chain specific, 1:3000, Chemicon,

Temecula, CA, USA), anti-human IgM (µ-chain specific, 1:5000,

Chemicon, Temecula, CA, USA) or anti-human IgA (α-chain

specific, 1:10000, Sigma, St. Louis, Mo, USA) were used as

secondary antibodies and incubated at 37°C for 1 h. Three washes

were performed using the washing solution and a chromogen

substrate solution (Sigma FAST TM OPD, Sigma Aldrich, St. Louis,

MO, USA) was added. After a 30 min reaction at room temperature

in the absence of light, the reaction was terminated using 1 N

sulfuric acid. The microplate was read at A492 using a semiautomatic

ELISA plate reader.

Statistical analysis

The data was analyzed using the t test. The statistical analysis was

performed using commercially available software (Statistical

Package for the Social Sciences, version 10.0, SPSS Inc., Chicago,

IL, USA). Differences between the experimental and control group

were considered to be statistically significant, when the P value was

0.10 A B

IgM detection (O.D. 492 nm)











IgG detection (O.D. 492 nm)







Martinez-Guzman et al. 13

.4 .6 .8 1.0 1.2 1.4 1.6 1.8 2.0 2.2 2.4

.4 .6 .8 1.0 1.2 1.4 1.6 1.8 2.0 2.2 2.4

.5 Patients .7 .9 1.1 1.3 1.5 1.7 Control 1.9 2.1 2.3 2.5

.5 .7Patients

.9 1.1 1.3 1.5 1.7 Control

1.9 2.1 2.3 2.5


IgA detection (O.D. 492 nm)






.4 .6 .8 1.0 1.2 1.4 1.6 1.8 2.0 2.2 2.4

.5 .7 Patients .9 1.1 1.3 1.5 1.7 1.9 Control 2.1 2.3 2.5

Figure 2. Presence of antibodies against cell extract from Porphyromonas gingivalis ATCC 33277. A) 9 patients with chronic periodontitis

shown IgM levels up controls b) 6 patients had IgG antibodies and c) 13 patients had IgA antibodies against semi-purified culture filter


periodontitis patients (that is the same proportion as that

revealed for IgG antibody), IgA antibody was detected in

the saliva.(Figure 1).

IgA, IgM and IgG antibodies anti-extract cell from P.

gingivalis in saliva and gingival crevicular fluid by


In 31.0% of chronic periodontitis patients, IgM antibody

was detected in the gingival crevicular fluid. In 20.7% of

chronic periodontitis patients, IgG antibody was detected

in the gingival crevicular fluid. Finally, in 44.8% of chronic

periodontitis patients, IgA antibody was detected in the

saliva (Figure 2).


Periodontal diseases comprise a heterogeneous group of

infections that are caused by microorganisms that

colonize the tooth surface in the gingival crevicular area

(Loesche and Grossman, 2001). Inflammation of the

gingiva extending into the adjacent attachment apparatus

is known as chronic periodontitis and is characterized by

loss of the periodontal ligament and the adjacent

supporting alveolar bone (Loesche and Grossman, 2001;

Caton and Greensteinm, 2000, 1993). Microorganisms,

host response, and environmental factors are involved in

or associated with the pathogenesis of periodontitis

(Haffajee et al., 1995). The presence of certain specific

periodontal pathogens, such as P. gingivalis, has been

associated with periodontal tissue breakdown and

progression of periodontitis (Haffajee and Socransky,

2000; World Workshop in Periodontics, 1996; Haffajee

and Socransky, 2000, 2005; Socransky et al., 1998;

Laemmli, 1970). Antibody detection with enzyme-linked

immunosorbent assay seems to reflect both past

exposure and present level of bacterial challenge

(Bascones and Figuero, 2005; Haffajee et al., 1995).

Animal models have been used in the humoral immune

response evaluation in periodontitis (Towbin et al., 1979;

14 J. Infect. Dis. Immun.

Socransky and Haffajee, 1992).

In a study, high levels of IgG and IgM antibodies were

found in mice after P. gingivalis immunization with whole

or the outer membrane fraction using ELISA (Gemmell et

al., 2004). In this study, IgA, IgG and IgM antibodies were

detected against semi-purified culture-secreted proteins

and extract cell from P. gingivalis. In another study,

immunodominant antigens from P. gingivalis ATCC

33277 in whole-cell sonicates, proteinase K-digested

sonicate, lipopolysaccharide, capsular polysaccharide,

and whole-cell protein fractions were studied and it was

revealed that whole-cell protein fraction was

immunodominant and induced a more effective

antibodies response (Leone et al., 2006). In other

studies, several immunodominant antigens were

demonstrated to be present in extract cell from P.

gingivalis, which have a molecular weight of 55 and 40

kDa (Kesavalu et al., 1992; Chen et al., 1995). It is

possible that those antigens could induce the production

of antibodies at a local or systemic level in humans. The

levels of IgG and IgM antibodies in gingival crevicular

fluid were not significantly different between periodontitis

patients and healthy controls. This finding could be

explained by:

1. The low number of patients enrolled in the study, which

was a limitation of this study; and

2. Most antibodies are forming immune complexes and

thus stimulating the inflammation process.

IgG antibodies found in healthy controls could indicate an

immunological memory protecting the host from P.

gingivalis infection. IgM detection in experimental group

is indicative of an active infection by P. gingivalis.

Proinflammatory cytokines have been associated with

destruction in periodontal tissues in patients, in which

antibodies to P. gingivalis were not found (Chen et al.,

1995). In conclusion, the present study supports the

concept of a dual role of the humoral immune response:

First, a protective effect of IgG antibodies and, second,

the probability that immune complexes might have a

destructive effect upon periodontal tissues in patients

with low levels of antibodies in gingival crevicular fluid,

while IgM levels are high. This study demonstrated a

potential application of ELISA test to detect bacterialspecific

antibodies in the gingival crevicular fluid and its

use at least in P. gingivalis detection.


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