Vol.1, No.3, 112-120 (201 1)
opyright © 2011 SciRes. Openly accessible at http://www.scirp.org/journal/OJAS/
Open Journal of Animal Sciences
Basic biological aspects of Tritrichomonas foetus of
relevance to the treatment of bovines suffering of
Newton Soares da Silva1,3*, Susane Moreira Machado1, Fernando Costa e Silva Filho2,
Cristina Pacheco-Soares1,3
1Laboratório de Bi o l o g ia Celular e Tecidual, Instituto de Pesquisa e Desenvolvimento, Universidade do Vale do Paraíba, São José dos
Campos, São Paulo, Brasil; *Corresp onding Author: nsoares@univap.br
2Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, CCS - Bloco G, Rio de Janeiro, Brasil;
3Laboratório de Dinâmica dos Compartimentos Celulares, Instituto de Pesquisa e Desenvolvimento, Universidade do Vale do Paraíba,
São José dos Campos, São Paulo, Brazil.
Received 8 June 2011; revised 14 July 2011; accepted 25 July 2011.
Tritrichomonas foetus is a flagellate protozoan
and the etiological agent of bovine genital
trichomoniasis [1], which is an infectious vene-
real disease. This parasite is usually found as-
sociated with the mucosal surface of the uro-
genit al tract in females or the male preputial and
penile membranes. In females, the clinical
manifestations may include abortion, with repe-
tition of estrus at irregular intervals, vaginitis,
cervicitis, endometritis, and pyometra. Parasi-
tized males may have a discharge with small
nodules in the preputial membrane. After that,
the bulls have no clinical symptoms, and are
thus an asymptomatic carrier that may spread
the infection. Considering that a bull could
cover up to twenty females [2], bovine genital
trichomoniasis is a serious medical and veteri-
nary problem, with economical repercussion for
beef and milk production. As T. foetus is an
amitochondrial and aerotolerant organism, en-
ergy production under low O2 tension in the
protozoan is done via hydrogenosome, which,
as the name suggests, is the organelle where H2
is generated [3,4,5]. The molecular machinery of
mitochondrial cell death is, therefore, absent in
this parasite and the mechanism that activates
of cell death program is not clear. This review
seeks to understand the characteristics of the
protozoan parasite T. fo etu s in order to propose
new therapies for animals suffering from this
infectious and contagious agent.
Keywords: Reproduction; Protozoan Parasite;
Tritrichom on as foetus
Tritrich omonas foetus, Reidmüller 1928 emend. Kirby
1947, is a flagellate protozoan that lives in oxygen-poor
environments, such as the bovine reproductive tract [6].
This protozoan is found in the urogenital mucosal sur-
face of males and females, causing bovine trichomoni-
asis, an infectious disease with venereal transmission,
which causes infertility and abortion in cattle increasing
herd management expenses [7,8]. Trichomoniasis is pro-
bably the third most common cause of abortion in cattle
(after Brucellosis and Leptospirosis) [7]. This disease
has worldwide distribution [8], and is endemic especially
in regions with poor sanitary control or where the use of
natural mating for reproduction is extensive [9].
T. fo etus is physically associated with the epithelium
lining the urogenital cavities of cattle [10,11]. In bulls,
the parasite can be detected in the preputial cavity and
urethra, as well as in the urogenital canal [11,12]. In cows,
it inhabits the vagina and uterus, in which the parasite
can inhibit the attachment of embryo or rupture its mem-
branes after attachment, leading to abortion [10,11,13].
Despite the economic importance attributed to bovine
trichomoniasis, there have been few studies about the
molecular basis and chemotherapy of disease, thus it has
failed to be eradicated, or even rigorously control. There-
fore, the disease continues to cause problems for Brazil-
ian and other cattle [9].
1.1. Morphofunctional Characteri stics of T.
1.1.1. General Aspect s
Tritrichomonas foetus Kirby, 1947 belongs to the
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family Trichomonadidae, order Trichomonadida Kirby,
1947, class Zoomastigophora, subphylum Mastigophora,
Sarcomastigophora, phylum Sarcomastigophora, sub-
kingdom Protozoa, and kingdom Protista [14].
Tritrichomonas foetus, Tritrichomonas suis (parasite
of the digestive tract and nasal cavity of pigs) and Tri-
trichomonas mobilensis (parasite of the digestive tract,
especially the cecum and colon in monkeys) were found
after analyzing gene sequences to probably be strains or
variants of the same species [10,15,16].
T. foetus is a monogenic and monoxenic protozoan,
which is aerotolerant and actively mobile. It reproduces
by binary division and in vitro, axenic culture. The pre-
dominant form of trophozoite is approximately 10 to 25
m long by 3 to 15 m wide. However, both in vitro and
in vivo or in situ, the parasite has morphology that varies
from pyriform to fusiform or even round. It characteris-
tically has three free anterior flagella and a quarter, an-
teroposterior projection , which is occasionally associated
with the plasma membrane, resulting in a stru cture known
as the undulating membrane. This, in turn, is associated
internally to coast. The axostil, an organelle formed by
parallel bundles of microtubu les and anteroposter ior pro-
jection, projects itself externally in the form of terminal
spine [10]. Axostil and pelta, parts of the cytoskeleton,
together with the coast and flagella are jointly involved
in motor functions and cell division of the parasite
[10,17]. The other intracellular structures of T. fo etu s are
the parabasal body (Golgi apparatus and parabasal fila-
ments), the oval nucleus (located in the anterior third of
the body), and hydrogenosomes (functional replace-
ments of the mitochondria). The cytoplasm also has a
wide variety of vacuoles and vesicles related to the en-
cytosis, digestion, and transport processes, as well as
rough endoplasmic reticulum, free ribosomes, and gly-
cogen granules [17]. The nutrient uptake in T. fo etu s can
occur by diffusion as well as by phagocytosis and pino-
cytosis, resulting in the formation of cytoplasmic vacu-
oles of various sizes [17]. In vitro in ax enic and acellular
culture, T. foetus uses glucose as the principal energy
precursor. Even in vivo, where the supply of sugar is
almost nonexistent in the initial infection sites, the para-
site makes use of precursors in the synthesis of poly-
amines, such as arginine, to produce the energy needed
to survive in the host [18,19].
1.1.2. Particular Point, the Cell Surface
The first region the parasite contacts the host envi-
nment is on its surface. Therefore, this organelle plays a
crucial role in the etiology of bovine trichomoniasis.
From a structural viewpoint, it is defined as a cell surce
organelle formed by the plasma membrane and exterlly
associated carbohydrates. Studies that focus on tricomo-
ds-host cell interaction have shown that the cytotoxicity
of T. foetus can be triggered from physical contact be-
een the surfaces of the parasite and host cell, resulting in
the secretion of extracellular proteases and glycosidases
[20-22]. Such enzymes, in turn, seem not only to induce
cytolysis or the disruption of epithelial junctions, but to
remodel the surrounding extracellular matrix (ECM)
[23]. Thus, mechanochemical monitoring of the ex-
tracellular environment by the surface of the parasite
would co-opt the host’s ability to constitute a niche and
thus to survive in various anatomical sites.
From a molecular standpoint, the surface of tricho-
monads is a mosaic composed of cytopathic and cyto-
toxic enzymes, lectins, adhesins, receptors, and co-recep-
tors for ECM components, as well as other molecules
involved in adhesion and toxicity of host cell trichomo-
nads [22-28].
Adhesins and cysteine proteases on the surface of T.
foetus are directly involved in parasite interaction with
host cells. A 100-kDa protein characterized as adhesin
has been observed throughout the cell surface of T. fo e -
tus, mainly in the region of the flagella [29]. Cysteine
proteases, soluble or associated with the surface of T.
foetus, are have more cytotoxicity than the cytoad hesion.
These proteins induce apoptosis in bovine vaginal
epithelial cells (BVECs), which suggests that this mecha-
nism of cell death may be involved in the pathogenesis
of these protozoa [30].
A surface molecule of 118 kDa enables T. foetus to
recognize laminin-1, which is component of ECM of the
base membrane of epithelia. The immobilized or solub le
fibronectin is also recognized by T. foetus via surface
glycoconjugates rich in mannose [22,27]. Thus in prin-
ciple, the T. foetus host could not only lyse epithelial
cells or break its junction al complexe s, it may recogn ize
the ECM host and destroy or reshape it in a timely basis
thereby winning in other situations.
Lectins on the surface of T. foetus are related to the
recognition of portions of oligosaccharides of glycocon-
jugates on the surface of epithelial cells [22]. Moreover,
lectins, together with fluorochromes conjugated or com-
plexed with colloidal gold, react with residues of D-
GlcNAc, N-acetyl-D-galactosamine, sialic acid, D-man-
nose, D-glucose, L-fucose, and D-galactose on the sur-
face the protozoan [20,24]. Together, these data seem to
indicate that, at least in vitro, lectins on the surface oli-
gosaccharides of T. f o e t u s could be involved in recogni-
tion and parasite adhesion to host cells.
1.2. Pathogenesis of T. foetus
1.2.1. Female Genit al Tract
After infection, virtually all of the genital tract be-
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comes contaminated within twenty days. Initially, the
parasite multiplies intensively in the vagina and is sub-
sequently located mainly in the folds of the uterine cer-
vix. Infection often leads to a moderate vaginitis with
purulent discharge, with or without mild endometriosis
and transitory infertility, leading to pyometra, salpingitis,
and cervicitis [10,13,31 ,32].
Protozoa are more numerous between 14 and 18 days
after infection. The inflammatory response of the uterus
occurs between six to eight weeks after infection and is
probably responsible for the death of the embryo. The
interruption of pregnancy is usually concentrated in the
first weeks of pregnancy, but may extend until the fifth
month. The uterus in some females do not become in-
vaded, and thus they can have normal pregnancies and
births [10,13,31,32].
From the vagina to the cervix, T. foetu s then invades
the uterus and grows in fetal membranes producing pla-
centitis, detachment, and death of the embryo, by direct
action of the protozoa or from the effects of the inflame-
mation [10,31]. The pathogenic mechanisms that cause
embryonic or fetal death have not been understood fully
yet. The inflammatory process can vary between acute
and chronic, characterized by accumulation of neutron-
phils, macrophages, lymphocytes, and occasionally
plasma cells. The inflammatory reaction that develops in
the host, causing changes in the uterine environment,
and cytotoxicity mediated by lymphokine, has been
suggested as possible mechanisms [10].
The deleterious effects that are caused by T. f oe tu s di-
rectly on the embryo or fetus have been demonstrated by
identifying cysteine proteases of the parasite in cer-
vico-vaginal mucus of experimentally infected cows.
These soluble proteases are directly associated with the
digestion of host secretions (albumin, fibrinogen) and
participate in the processes of iron absorption from lac-
toferrin [33], in cytoadhesion and acquired immunity
(immunoglobulins G1 and G2) [17,26,34].
Abortion of the calf usually occurs between the first
and third months of pregnancy, may exceptionally hap-
pen after the fifth or sixth months of pregnancy. When
there is a complete release of the placenta and fetal
membranes, female naturally recover. Retained placenta
with membranes can result in chronic catarrhal or puru-
lent endometritis and may result in permanent sterility
After the embryonic or fetal death occurs, a period of
gradual recovery usually restores uterine fertility within
two to six months after the initial exposure to the para-
site. If the corpus luteum and macerated fetus remain,
the female may develop pyometra, which can cause
permanent infertility. The corpus luteum is maintained
active, probably due to lack of prostaglandin secretions
by the endometrium [17].
In females, the infection is self-limiting, lasting an
average of 90 - 95 days, but during that period they may
continue transmitting the parasite to bulls through
breeding activity [13]. Infected cows harbor the parasite
for several estrous cycles or after the termination of
pregnancy. T. foetus is then removed from the uterus,
cervix, and vagina, because of a specific infection in-
duced immune response. However, such immunity is not
permanent and females are subject to subsequent rein-
fections in coitus [17].
1.2.2. Male Genit al Tract
In the bull th e parasite is found on the p enis, preputial
cavity, and in some cases, the urethral opening. Penile
mucosa and adjacent areas of the preputial mucosa have
a large concentration of protozoa, which are not invasive,
situated in the surface mucosa, in secretions and the
glandular light [10,12,35,36,37].
Infected bulls serve as carriers of the parasite and in
older animals the infection becomes chronic, possibly
because of the increase in the number and depth of the
villi of the prepu tial epithelium in these animals [10,38].
Younger males are less likely to become permanent car-
riers of the infection in relation to older, nevertheless,
they are capable of transmitting the parasite to suscepti-
ble females [10].
Typically, males exhibit no macroscopic evidence of
infection due to the presence of the parasite, but can re-
main as carriers throughout their lives, unless they are
medicated. There are rare cases of balanitis and acro-
bustite. These problems, if present, are more of cones-
quence of associated infections than from the action of
the parasite. Histopathological examination of the subepi-
thelial area of the penis and foreskin reveals the presence
of a moderate infiltration of neutrophils, macrophages,
and lymphocytes, which are often accompanied by an
increased number of plasma cells [10,12,36].
1.3. Immunological Aspects
Studies on the immune response to infection by T.
foetus in bulls are scarce. The fact that young animals
are more resistant to infection is related more to the mi-
croscopic structure of the lining of the penis and foreskin
than an effective immune response, which is probably
absent in these animals [10,38].
Females are able to develop an effective immune re-
sponse against T. foetus. The parasite stimulates a mild
inflammatory response associated with the interruption
of pregnancy. Inflammation is mediated by an immune
mechanism that often eliminate the infection [17]. In
carrier cows, this immune mechanism probably fails,
maintaining the infection in the herd [32].
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After the initial infection with T. foetus, bovine fe-
males respond with the local secretion of immunoglobu-
lins IgG and IgA in cervico-vaginal mucus secreted by
the uterus. The elimination of infection is probably me-
diated by specific immunoglobulins, since the organism
is an extracellular parasite. Monoclonal an tibodies cause
agglutination and complement mediated lysis that pre-
vent the adhesion of parasites to the epithelial cells of
the vagina, thereby facilitating phagocytosis of T. f o e t u s
by monocytes. The association between specific anti-T.
foetus antibodies and complement potentiates the death
of the parasites by polymorphonuclear leukocytes
1.4. Treatment
Females with T. f oe t us are able to eliminate the infec-
tion without therapy, after the adoption of sexual absti-
nence for ninety days and normal uterine involution.
Females who manifest post-coital pyometra should re-
ceive appropriate care aimed at the corpus luteum re-
gression and elimination of uterine content [8]. Animals
with untreated pyometra can become permanently sterile,
which would justify their disposal [17].
The treatment of bulls infected with T. fo etu s has been
proposed by some researchers as a complementary
measure to eradicate the disease in the herd. However,
currently there is no effective drug approved for the
treatment of males and females infected with T. foetus
and the results have not always been satisfactory [8].
Two different forms of treatment are recommended
for infected males: topical of the preputial and penile
membrane and oral. However, treatments are usually
lengthy, often requiring many repetitions, and have
varying degrees of side effects such as tissue destruction,
loss of appetite, and digestive disorders in orally admin-
istered pro ducts [8,17].
Employment of trichomonicidal agents, preferably in
bulls, is justified by the fact that these animals are the
disseminators and hosts of the parasite. In females, sex-
ual abstinence for ninety days can eliminate T. foetus.
Topical, drugs have been tested with several active in-
gredients in the elimination of T. fo e t u s , such as acrifla-
vine associated with tripaflavine and acriflavine [17].
Orally, imidazole derivatives have been tested, such as
metronidazole, ipromidazole, and dimetridazole, with
varying results [17,41]. Treatment is not recommended
for a large number of bulls or to be used indiscriminate
in a herd, but should be restricting to high value live-
Diseases caused by tricomonads can be cured by the
use of 5-nitroimidazoles such as metronidazole, effective
against various anaerobic and aerotolerant microorgan-
isms [42]. Via glycolysis, the decarboxylation of pyru-
vate to hidrogenosomas T. f oe tu s is coupled to ATP syn-
thesis and linked to electron transport mediated by fer-
ridoxin. This pathway is responsible for metabolic acti-
vation of 5-nitroimidazoles [3,42]. The antimicrobial
effect of these drugs depends more on its interaction
with DNA, than its metabolic reduction in the microor-
ganism and the consequent generation of free radicals
Although resistance to metronidazole did not show
any alarming clinical problem, some data related to the
subject should be taken in to cons ideration. The results of
[8] and [44] demonstrated that in vitro and in vivo
trichomonads develop resistance in a short period of
time, at low drug concentrations. This is alarming be-
cause of the possibility of trichomonads resistant strains
arising due to inappropriate treatment regimen pre-
scribed to animals carrying the parasite, which seems to
have occured with T. f oe t us: strain KV1 MR > 100 [14].
Many if not most drugs used to treat patients with the
human and bovine trichomoniasis are nitroimidazole
derivatives (2, 3, 4, and 5-nitroimidazoles). Although
these drugs have different pharmacokinetics, their intra-
cellular mechanisms of action are based on reducing the
nitro grouping [3,45,46].
1.5. Photodynamic Therapy
Photodynamic therapy (PDT) uses th e combin ation of
a dye or chromophore (photosensitizer) and a light source,
usually a LASER [47]. Although PDT was originally
developed as a cancer therapy, it also has great therapeu-
tic potential for other mucocutaneous manifestation dis-
eases such as psoriasis, fungal infections, and bacterial
infections resistant to antibiotic treatments. Photody-
namic therapy with derivatives of phthalocyanines is
proving effective in inactivating viruses such as herpes
simplex [48,49,50].
The concept of PDT originated in 1900 when Oscar
Raab [51] demonstrated that free-living protozoa of the
genus Paramecium could be killed by prior incubation
with sensitizers and subsequent white light illumination.
However, the modern PDT originated with the studies by
Lipson and Schwartz in 1960. These investigators ob-
served that injection of hematoporphyrin in tissues of
cancer patients, induced the appearance of fluorescence
in neoplastic lesions, visible during surgical procedures
1.5.1. Photosensitizers
Photosensitizers are chromophors that absorb light
energy at specific wavelengths and are able to induce
reactions in nonabsorbent molecules [52]. A variety of
synthetic photosensitizers has been proposed as the sec-
ond generation, for example, phthalocyanines and chlo-
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rins. Studies using these photosensitizers have been de-
veloped in order to eliminate problems associated with
the first generation photosensitizers, which have cuta-
neous photosensitivity and make inefficient use of light
at a low penetration wavelength [53].
The phthalocyanines induce sensitivity to radiation in
the wavelength range between 600 - 1.200 nm, which
can be conjugated to a variety of metals such as alumi-
num and zinc, increasing their lifespan and improving
photodynamic toxicity. The presence of side groups in
these photosensitizers can change its electrostatic charge
and solubility, thereby affecting its uptake by eukaryotic
cells. The increase in the sulfonation level of phthalo-
cyanine progressively reduces its affinity for lipid bilay-
ers, making it less phototoxic to mammalian cells. The
association of the photosensitizer with the lipid bilayer
may be more important than the amount of reactive
oxygen produced [53,54].
The transport of th e phthalocyan ine, in vivo, is usu ally
performed by low-density lipoprotein (LDL). LDL is re-
cognized by receptors on the plasma membrane. The
greater the number of receptors for LDL, the greater the
incorporation of photosensitizing will be and thus of
photodynamic therapy. The incorporation of sensitizers
is higher in cells with high mitotic rate, such as tumor
and endothelial cells. The phthalocyanine-LDL complex
binds to receptors on the plasma membrane and then is
internalized via endocytosis. In the intracellular envi-
ronment, LDL-phthalocyanine is usually in addition to
the plasma membrane, in lysosomes and mitochondria
1.5.2. Photodestruction Mechanism
Photodynamic therapy is characterized by celular
photooxidation v ia prior sensitization of th e cell with the
photosensitizer present in the target tissue. While many
of these photosensitizers may be natural constituents of
the tissues, as the first step of treatment, they should be
introduced into tissues by direct administration. In the
second step, the tissue containing the photosensitizer is
irradiated with laser, at the wavelength of maximum
absorption of the first. The light interacts with the pho-
tosensitizer. In this state, the half life of the photosensi-
tizer is a few millionths of a second, long enough for it
to quickly energize the dissolved oxygen, resulting in
production of reactive oxygen species or ROS, such as
1O2, H2O2, OH-, and O2–. Such species are chemically
unstable and highly reactive, which generally causes
eukaryotic cell death. Various structures and organelles
can be targets for PDT, including the plasma membrane,
nucleus, mitochondria, Golgi apparatus, lysosomes, and
cytoskeletal structures [56,57].
1.6. Cell Death, Necrosis and Apoptosis.
Programmed cell death (PCD) is a genetically regu-
lated physiological process in the development and ho-
meostasis of multi and unicellular organisms [58-61].
Once scientists recognized that organisms are composed
of cells, they discovered that cell death could be an im-
portant part of life. First observed during the metamor-
phosis of amphibians, cell death was soon discovered in
the normal development of many tissues of both inver-
tebrates and vertebrates [62]. Today, cell death is known
to be a remarkable and essential event both in normal
cells of organisms and in pathophysiological processes,
which can cause diseases [63].
The term “programmed cell death” has been used to
describe cell death that occurs in predictable places and
times during development, emphasizing that deaths are
somehow programmed during the development plan of
the organism [62]. Subsequently researchers determined
that the process of cell death is the main mechanism
controlling the number of cells (differentiation, embryo-
genesis, metamorphosis, and aging). It also acts in the
defense mechanism to remove unwanted cells, which
may even potentially be dangerous to the body, and pre-
vent several diseases including cardiomyopathy and
cancers [62,64-66]. In some cases, there is degradation
of an entire cell, other times it occurs on a subcellular
scale due to lack of food in which the cell needs to de-
grade proteins and certain non-essential organelles to
recycle these compounds for reuse in the c ytosol [66 ].
The interest in the process of cell death began to grow
rapidly b y 1990 when there was a chang e in the descrip-
tion from, “the cell dies and is replaced” to a new point
of view that says, “cell death is not an incident of life,
but an important and highly controlled element of exis-
tence”. Thus, with the change of emphasis, cell death has
become recognized as an interesting biologi cal event [67].
In 1972, Kerr and colleagues (apud [65]), performed
classical ultrastructural experiments, which provided
evidence that the cells undergo at least two distinct types
of cell death: the first known as necrosis and a second
called apoptosis. This work led to interest in pro-
grammed cell death, first because it provided a visible
object (profile apoptosis) to be consistently focused on
previous experimental studies in relation to the disap-
pearance of dead cells and second ly it provided eviden ce
for the controlled events that justify th e operational defi-
nition of “pr ogrammed”.
In the last decade, apoptosis has attracted great scien-
tific interest. Significant progress has been made in un-
derstanding the factors that control survival and cell
death as well as the intracellular events associated with
the “suicide” cell. However, morphological and bio-
chemical evidence suggest that programmed cell death is
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not confined to apoptosis and necrosis. In many biologi-
cal systems, cellular suicide has shown the involvement
of a lysosomal autophagic compartment. Thus cell death
associated with autophagy has been observed in the
fungus Dictyostelium discoideum during induction of
nutritional stress; physiological stages of development,
such as metamorphosis in insects,embryogenesis in
mammals with regression of webbing and in adults pri-
marily in the intestine, mammary glands, and ovarian
follicles [68].
The clinical implications of understanding program-
med death are significant. Identified program compo-
nents of signal transduction in PCD are potential targets
for drug development and new therapies that might acti-
vate the cell death program, thereby help ing to eradicate
pathogens by antib iotics.
Mariante [69] observed that hydrogen peroxide (H2O2)
induced activation of caspases and a mechanism of pro-
grammed cell death in T. foe tu s. The authors report that:
(1) H2O2 led to loss of motility and induced cell death, (2)
dead protozoa exhibited some characteristics similar to
those found during cell death of other organisms, (3) a
“caspase-like” protein appears to be activated during this
process of cell death. They proposed that although T.
foetus did not show any mitochondria or known cell
death pathway, it is likely to have some mechanism of
cell death. T. f oe t us exhibited morphological and physio-
logical changes in response to treatment with H2O2. To-
gether, these results suggest that a cell death pathway,
involving at least o ne member of the fami ly of caspases,
can exist in amitoco ndrials bodies such as trichomonads.
The hydrogenosome has an important role in the oxida-
tive burst in trichomonads and is a candidate to partici-
pate in this event [69 ].
In amitochondrial organisms, such as trichomonads, it
has been assumed that the machinery of PCD is absent,
but studies by [70] led to the proposal that the existence
of both caspase-dependent and caspase-independent
mechanisms of cell death may be present in trichomo-
Preliminary results of PDT in T. foetus [71] the au-
thors observed ultrastructural changes, such as project-
tions of the plasma membrane, nuclear fragmentation
with masses of heterochromatin in the periphery, prolif-
eration of endoplasmic reticulum, intense vacuolization
of cytoplasm, and complex and fragmented axostilar
pelta-internalization of flagella. These results were also
observed in [69] after treatment with H2O2, suggesting
that oxidative stress induces a mechanism of cell death
in this parasite.
In animals, the PCD is associated with the elimination
of super cells expressed in the development and eradica-
tion of others, defective [72]. Teratogenic transforma-
tions, microbial infections, lethal factors such as heat,
mutagens and oxidants agents, and toxins induce the
activation of PCD. Recent studies have shown the exis-
tence of PCD in unicellular eukaryotes of different phy-
logenetic origins, indicating that the conservation of the
molecular mechanism is relevant to the functional ro le of
this process in the biology of protozoa [69]. The possible
reasons that the apoptosis pathways in protozoa are
comparable to those of yeast and bacteria may be to (a)
protect populations of healthy cells, (b) obtain nutrients
from neighboring cells committing altru istic suicide, and
(c) decrease pe rpetuation of mutatio ns.
Here, we briefly review some T. foetus properties
which are relevant to the development of new treatments
directed towards bovine cattle suffering of trichomoni-
asis. Several drugs have been used to investigate the
cytotoxic effect on T. foetus, such as colchicine, vin-
blastine, cytochalasin B [27], taxol, nocodazole, griseo-
fulvin, lactacyst, and hydrogen peroxide [73]. Da Silva
et al. [71] analyzed the cytotoxic effect produced by
PDT with aluminum phthalocyanine tetrasulfonated
(AlPcS4) photosensitizer on T. foetus culture. They
demonstrated that PDT killed an amitochondrial organ-
ism such as T. foetus. In this parasite, PDT induces a
type of cell death other than necrosis. Apoptosis or
autophagic cell death after PDT in T. f oe t us may benefit
bovines by limiting the inflammatory response, which is
detrimental and could even be lethal to these animals.
We believe that the results obtained from the study of
new therapies such as PDT explained in this article will
bring benefits to the treatment of cattle suffering from
trichomoniasis. This treatment would be without side
effects, which are characteristic of antimicrobial therapy
with nitroimidazoles.
This work has been supported by FAPESP (2008/06654-4), CNPq
(309699/2009-6) and CNPq-INCT/INPeTAm (573695/2008-3).
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