One Health is a collaborative, multisectoral, and transdisciplinary approach — working at the local,
regional, national, and global levels — with the goal of achieving optimal health outcomes recognizing
the interconnection between people, animals, plants, and their shared environment.
One Health is an approach that recognizes that the health of people is closely connected to the health of
animals and our shared environment. One Health is not new, but it has become more important in
recent years. This is because many factors have changed interactions between people, animals, plants,
and our environment.
Human populations are growing and expanding into new geographic areas. As a result, more people live
in close contact with wild and domestic animals, both livestock and pets. Animals play an important role
in our lives, whether for food, fiber, livelihoods, travel, sport, education, or companionship. Close
contact with animals and their environments provides more opportunities for diseases to pass between
animals and people.
Diseases:
Anthrax, Brucellosis, Bovine tuberculosis, Listeriosis, Salmonellosis, Leptospirosis, Camphylobacteriosis,
Cat scratch disease and Psittacosis
Gram-negative bacteria cause infections including pneumonia, bloodstream infections, wound or
surgical site infections, and meningitis in healthcare settings. Gram-negative bacteria are resistant to
multiple drugs and are increasingly resistant to most available antibiotics.
Yersinia pestis:
Characteristics:
Y. pestis is a gram negative, rod shaped and facultative anaerobic bacteria. It is non-motile, non-spore
forming and exhibit bipolar staining. It grows less rabidly and has an incubation period of 72 hours, at
optimum 37°C. Biochemical characteristics: Lactose and hydrogen sulfide negative, urease negative and I
M positive Vi negative C negative.
Virulence Factors:
Plasmid: It encodes genes for expression of several virulent factors.
Chromosomal encoded virulence factors: Like plasmids, chromosomes also with-hold some genes for
virulent factor expression. But plasmid have a more prominent role in case virulence.
Antiphagocytic Protein Capsule: Antigen F1 and Antigen V are produced by the bacterium once inside a
macrophage. These prevent phagocytosis by the host macrophage.
Type-III secretion system (T3SS) creates holes (YopB & D) in the immune cells (mostly macrophages) and
cause cytolysis. Non-cytolyzed immune cells injected (YopO, H, M, J, T) with T3SS prevents phagocytic
activity.
YopH: It is a protein tyrosine phosphate helps bacterium evade the immune system.
YopE and Yop T: Limit cytolysis of the white blood cell caused by pore formation from YopB and YopD.
YopJ is acetyltransferase that induces apoptosis in the macrophage cell which helps the bacterium
escape immune responses.
YopO is a protein kinase that induces apoptosis in macrophages.
YopM down regulates leukocyte recruitment and inflammation.
Plasminogen activator: Important factor in pneumonic plague where it may help in systemic invasion by
degrading blood clots.
Endotoxin: This is responsible for systemic effects of the disease.
Zoonotic Disease:
Y. pestis cause plagues in human beings. The yersinia infection can be pneumonic, bubonic or
scepticemic inn form. The reservoir host for plague are rodents especially rats and mice infested with
fleas (Xenopsylla cheopis).
Brucella melitensis:
Characteristics:
B. melitensis are small bacteria that are gram negative Non-motile coccobacillary rods. They are aerobes
acid fast organisms that are intracellular pathogens. They are extremely slow growing bacteria with an
incubation period of 3 to 5 days in optimum 37°C. Their colonies are small, smooth, glistening,
translucent and non-hemolytic, and have bluish color.
Biochemical characteristics: Catalase, Urease and Oxidase positive while Hydrogen sulfite negative. In
host, they infect and proliferate macrophages but are unable to do so in neutrophils.
Virulence Factors:
Capsule: In Brucella strains that have rough colonies, they are less virulent as compared to the strains
forming smooth colonies. The capsule helps against phagocytosis by host cells.
Lipopolysaccharide: It consists of lipid A oligosaccharide core and Antigen O. They are responsible for
invading the macrophages while evading the immune surveillance of the host human or animal. These
lipopolysaccharides are relatively less virulent than the ones on other Gram negative bacteria like E. coli.
Type IV Secretion System (T4SS): It is a multiprotein complex that helps in the secretion of
macromolecules from bacterial cell. They help the bacteria invade the endoplasmic reticulum (ER) by
forming Brucella containing vacuole (BCV) which later interacts with ER.
Superoxide dismutase: These are defensive tool to against macrophage reactive oxygen species released
against the bacteria.
Catalase: It also helps against the macrophage reactive oxygen species by converting hydrogen per oxide
into oxygen and water.
Cytochrome oxidase: This enzyme helps the bacteria to survive inside the macrophage without being
digested.
Nitric Oxide Reductase: This enzyme helps the bacteria in two ways. Firstly it neutralizes the Nitric Oxide
produced from macrophages by converting it into oxygen and nitrogen. Secondly, the oxygen produced
by the neutralization fulfills oxygen demand for bacteria, especially in deficiency of oxygen.
BvrR and BvrS System: This system of proteins basically helps bacterial cell in invasion, inhibition of
phagosome-lysosome fusion and intracellular replication.
Neurotoxic Clostridium:
This group includes C. tetani and C. botulinum. C. tetani has single antigenic exotoxins for all strains.
Toxins of C. tetani:
Pathogenicity: They infect local area with the help of other bacteria that produces suitable environment
for their local survival and proliferation. Their exotoxins act in regions far away from the bacteria and
produce their effect.
Plasma mediated neurotoxin (tetnospasm): it is a heat labile exotoxin that acts systemically on the body.
Heat stable Haemolysin: It hemolyzes blood.
Mode of Action: The released toxin binds to the endings of peripheral nerve. They get internalized and
then travel to the spinal cord via retrograde intra-axonal transport. It negatively influences the activity
of inhibitory neurons blocking the inhibitory neurotransmitters release. It continuously stimulates by
excitatory transmitters and cause Spastic Paralysis. In general the toxin causes spastic paralysis, lock jaw,
cardiac arrhythmia and blood pressure fluctuations. The toxins produced in wounds can also produce
effects by traveling systemically.
Toxins of C. botulinum:
There are 7 antigenically unique toxins identified for botulism. These are toxin A, B, C, D, E, F and G.
Somatic antigens are heat stable and heat labile
More specific are the spore antigens.
Pathogenicity: These are phage mediated toxins that are regulated by the genome of the bacteria.
These neurotoxins (botulin) act systemically and are released as a consequence of cell lysis.
Toxins A through G can cause lethal food borne intoxications.
Mode of Action: At the neuromuscular junction in cholinergic nerve endings, they bind to certain
receptors and block the release of Acetylcholine. This blocks the muscle stimulation and causes Flaccid
Paralysis..
virulence Factors:
Infectious Coryza:
Virulence factors of Haemophilus bacteria are mostly unknown or not well recognized. Some of them
include:
Endotoxins: Damage the cells and tissues of the host.
Outer Membrane Proteins: Cause spread of the organism in the host body.
Chronic Respiratory Disease:
Antigens: Some antigens of the Mycoplasmas are similar to the antigens of host tissues. The similarity is
so uncanny that they are able to evade the host immune system and cause persistant infection for a
long time. In case of immune system activation against mycoplasmas, chances of autoimmune disease is
substantially increased due to similarity in antigens.
Adhesion Protein: These help in adhesion of bacteria with host cell and occurs in only a few mycoplasma
strains.
Toxins: These are usually soluble factors that the bacterium uses to cause damage to cells.
Flexible Outer Membrane: They lack a cell wall but possess a thick three layerd and flexible outer
membrane that helps them avoid phagocytosis.
ANTHRAX
Diagnosis:
And text me with ignores buy a microscopy culture an email inoculation serological demonstration of
anthrax antigen in infected tissue.
Antibodies organism can be demonstrated by gel diffusion, n compliment fixation antigen coated tanned
red cell agglutination and elisa techniques
An animal is suspected to have died of anthrax autopsy is not permissible as the spilt blood will lead to
the contamination of soil
Any year may be cut off from the carcass. and sent to the laboratory alternatively swab soaked in the
blood or several blood smears may be sent.
The demonstration of gram positive bacilli with the morphology of anthrax bacilli and a positive
M'Fadyean 's reaction will enable presumptive diagnosis to be made.
Immuno fluorescent microscopy can confirm the identification.
The CDC have prepared guidelines for identification of anthrax bacillus.
Any large gram positive bacilli as with the general morphology and cultural features of anthrax non
motile nonhemolytic on blood agar and catalase positive can be given a presumptive report of anthrax.
For initial confirmation lysis by gamma phage and d essay for capsule specific staining and for
polysaccharide cell wall antigen are sufficient.
For further confirmation PCR for anthrax bacillus specific chromosomal marker can be done.
For epidemiological studies and strength characterization MLV A and AFLP cann be used.
Treatment:
Antibiotic therapy is effective in human cases but really succeeds in animal as therapy is not started
sufficiently early
antibiotic have no effect on the talks in once it is formed
penicillin and streptomycin are no longer used for treatment they have been replaced by Doxycycline
and ciprofloxacin which are effective in prophylaxis and treatment..
Bovine TB:
In live cattle tuberculosis is usually diagnosed in the field with the tuberculin skin test.
In this test tuberculin is injected intradelhi a positive test is indicated by a delayed hypersensitivity
reaction (swelling)
Tuberculin test can be performed using bovine tuberculin alone or as a comparative test that
distinguishes reactions to M. Bovis from the reactions to environmental mycobacteria.
The caudal fold( bovine tuberculin) is used for the test for preliminary screening of cattle reactors are re
tested with the comparative cervical test..
False negative responses are sometime seen soon after infection in the late stages of the disease in
animal with the poor immune responses and in those that have recently calved.
LABORATORY DIAGNOSIS:
Are presumptive diagnosis can also be made by histopathology and the microscopic demonstration of
acid fast bacilli
direct smears from the clinical samples of tissues maybe stand with the nails in stain of fluorescent acid
fast stain or immuno peroxidases techniques.
The diagnosis is confirmed by the isolation of impervious on selective culture media. Mycobacteria grow
slowly and the cultures are incubated for 8 weeks growth usually become visible in three to six weeks
the Identity of organism can be confirmed with biochemical tests and cultural characteristics for
polymerase chain reaction assays.
The lymphocyte proliferation and gamma interferon assays are blood test that measure cellular
immunity .
En zyme-linked immunosorbent assays Maya antibody titres to M.bovis. however tests of humoral
immunity are generally of limited utility in cattle because titres are inconsistent and rise only in the late
stages of infection.
Treatment:
In humans if you have an active tuberculosis disease you will be probably treated with a combination of
antibacterial medications for a period of 6 to 12 months.
The most common treatment for active tuberculosis is isoniazid in combination with three other drugs
rifampin, pyrazinamide and ethambutol
Dermatophytes;
Dermatophytes cause dermatophytosis ringworm disease fungal infection of superficial dead keratinized
tissue of hair and skin infection will often track into the hair follicles leading to temporary alopecia
trichophyton veerucosum is the most common cause in the cattle although occasionally microscopic
species may be involved ringworm is an important zoonosis.
Dermatophytes are pigment red saprophytic organisms and were previously called Punjabi imperfecti
determines a species of etna interstar microsporum and trycophton and are found worldwide. They are
usually secondary Invaders and are able to penetrate all layers of skin but are generally restricted to the
keratin layer and its appendages therefore the condition is most often seen in subcuticular sites.
Microsporum ca.
is is the most common dermatophyte to infect small animals and will be the cause of 90% of a line
infections and 60% of canine infection trichophyton mentagrophytes affect around 30% of dogs
especially terrier breeds trichophyton very kosam cause most cause cases in cattle and sheep and
trichophyton equinum is the commonest cause in horses about 25% of wild hedgehog are carriers of
trycophytonerinacei which can also affect dogs and human.
Signs:
There will be circular ever irregularly scaly and crusty 50 and alopecia will be seen in this area due to the
broken hair shops and hair loss from inflamed region of skin follicular papules and first use will also be
present there will be a paraphilia red ring due to the dead fungi in the areas of inflammation at the
centre of lesion and viable fanjoy peripherally. There is usually a varying degree of pruritis.
Diagnosis:
Woods lamp can be used to shine UV light on to the legion and it will fluoresce in 50% of cases.
Therefore it is a good diagnostic tool in small animals but is not incredibly reliable if there is no
fluorescence it does not mean there are no dermatophyte or no microsporum.
Treatment:
Defected animal should be isolated and precautions should be taken to prevent human infection such a
wearing gloves hair should be clipped around the skin lesions. Also antifungal drugs such as griseofulvin
itraconazole and topical therapy can be done.
Aspergillosis is caused by several Aspergillus spp, especially A fumigatus and A terreus. A niger, A
nidulans, A viridinutans, A flavus, and A felis are being recognized more commonly with increasing use of
molecular techniques for identification. Aspergillus infection is found worldwide and in almost all
domestic animals and birds as well as in many wild species. It is primarily a respiratory infection that
may become generalized; however, tissue predilection varies among species.
Clinical findings:
In birds, aspergillosis (brooder pneumonia) is primarily bronchopulmonary, with dyspnea, gasping,
anorexia, and emaciation. Torticollis and disturbances of equilibrium are seen when infection
disseminates to the brain. Yellow nodules of varying size and consistency or plaque lesions are found in
the respiratory passages, lungs, air sacs, or membranes of body cavities. Furlike growth of fungus may
be found on the thickened walls of air sacs. In birds, aspergillosis (brooder pneumonia) is primarily
bronchopulmonary, with dyspnea, gasping, anorexia, and emaciation. Torticollis and disturbances of
equilibrium are seen when infection disseminates to the brain. Yellow nodules of varying size and
consistency or plaque lesions are found in the respiratory passages, lungs, air sacs, or membranes of
body cavities. Fur ike growth of fungus may be found on the thickened walls of air sacs.
In ruminants, aspergillosis may be asymptomatic, appear in a bronchopulmonary form, cause mastitis,
or cause placentitis and abortion (mycotic abortion). Mycotic pneumonia may be rapidly fatal. Signs
include pyrexia; rapid, shallow, stertorous respiration; nasal discharge; and a moist cough.In ruminants,
aspergillosis may be asymptomatic, appear in a bronchopulmonary form, cause mastitis, or cause
placentitis and abortion (mycotic abortion). Mycotic pneumonia may be rapidly fatal. Signs include
pyrexia; rapid, shallow, stertorous respiration; nasal discharge; and a moist cough.
horses, aspergillus cause (Guttural Pouch Mycosis) epistaxis and dysphagia are common complications
of gutturomycosis. Guttural pouch is characterized by a necrotizing inflammation and is thickened,
hemorrhagic, and covered by a friable pseudomembrane. Mycotic rhinitis characterized by dyspnea and
nasal discharge has also been described. Aspergillosis can be a rapidly fatal disease associated with
diffuse pulmonary invasion. Locomotor and visual disturbances, including blindness, may occur when
the infection spreads to the brain and optic nerve. horses, aspergillus cause (Guttural Pouch Mycosis)
epistaxis and dysphagia are common complications of gutturomycosis. Guttural pouch is characterized
by a necrotizing inflammation and is thickened, hemorrhagic, and covered by a friable
pseudomembrane. Mycotic rhinitis characterized by dyspnea and nasal discharge has also been
described. Aspergillosis can be a
rapidly fatal disease associated with diffuse pulmonary invasion. Locomotor and visual disturbances,
including blindness, may occur when the infection spreads to the brain and optic nerve.
Diagnosis:
Radiographs in dogs with nasal aspergillosis may show generalized radiolucence of the nasal cavity
secondary to turbinate tissue destruction. A diagnosis based on culture results alone is not appropriate,
because aspergilli are ubiquitous and can be isolated from the nasal cavities of healthy dogs. Positive
culture results should be supported by demonstration of narrow, hyaline, septate, branching hyphae
within lesions or by serological testsRadiographs in dogs with nasal aspergillosis may show generalized
radiolucence of the nasal cavity secondary to turbinate tissue destruction. A diagnosis based on culture
results alone is not appropriate, because aspergilli are ubiquitous and can be isolated from the nasal
cavities of healthy dogs. Positive culture results should be supported by demonstration of narrow,
hyaline, septate, branching hyphae within lesions or by serological tests.
Treatment:
In dogs, topical treatment is considered the treatment of choice for nasal and paranasal aspergillosis.
Several surgical techniques and drug regimens have been used with varying success. Clotrimazole
formulated in a polyethylene glycol base is generally considered the first line treatment. Enilconazole,
ketoconazole, itraconazole, fluconazole, voriconazole, and posaconazole are effective.
In horses, surgical exposure and curettage have been used to treat gutturomycosis. Topical natamycin
and oral potassium iodide have been reported effective in cases of Aspergillus infection. Itraconazole (3
mg/kg, bid for 84–120 days) has been reported effective in Aspergillus rhinitis in horses.Bovine mastitis
has been treated successfully with combined intra-arterial and intramammary
injection with miconazole.
