Download Zoonotic diseases - Yeditepe University

Zoonotic
diseases
Meral Sönmezoğlu, Assoc Prof
Infectious Diseases Department
Yeditepe University Hospital
Zoonoses
From the Greek:
Zoon:
Animal
Noson:
Disease
Diseases and infections which are
naturally transmitted between
vertebrate animals and humans
- WHO 1959
Learning objects
•
•
•
1. Know the general terminology and
main organisms
2. Know epidemiology and clinical
symptoms of main zoonotic diseases
3. Understand the importance of the
diseases
Definition
• Zoonosis are diseases of vertebrate animals that can
be transmitted to man: either directly or indirectly
through an insect vector.
• Zoonosis are a complex group of diseases caused by
a remarkable diversity of pathogenic microorganisms
that ordinarily reside and cause illness in the
nonhuman animal world
Defining criteria
introduction to the zoonosis include the following:
• a vertebrate reservoir exclusive of humans;
• transmission of the agent directly to people or
from products derived from the host animal or
through an arthropod intermediate;
• and a recognized infectious disease syndrome
in susceptible individuals
Zoonosis: Importance
– In addition to their natural occurrence
many of these microorganisms are
prime candidates as biological weapons
Animal ZOONOSIS Human
Health
Health
Zoonosis (Zoonotic Diseases) - all diseases
naturally transmissible from animals to man
Zoonoses
• Does NOT include
– Fish and reptile toxins
– Allergies to vertebrates
– Diseases in which animal-derived food
serves as a vehicle (e.g. hepatitis A
contaminated deli meat)
– Experimentally transmitted diseases
Zoonoses
• > 250 zoonotic diseases
• Multiple pets in the home
• Human-animal bond
• Exotic species as pets
Zoonoses: Common Diseases
Frequency – (CDC, 2003)
Salmonella
39,919
Lyme disease
18,991
West Nile (CNS)
2,862
Trichinosis
4
Zoonoses
• Zoonotic diseases can be severe, life
threatening, and contagious
• and can even warn of an emerging
epidemic or
• a possible bioterror act
Zoonoses
Spectrum of Disease Severity
Death = rabies
Severe illness = plague
Chronic illness = Q-fever
Mild illness = psittacosis
Zoonoses: Importance
• Economics
– Zoonotic disease are expensive
• Rabies post-exposure prophylaxis
• GI illness due to Salmonella or Campylobacter –
lost productivity, medical costs
– Import/Export
• BSE – restriction on cattle
• Avian Influenza – restriction on chicken
• Travel/Globalization
• Decreased transit time - SARS
• Remote area accessibility
Zoonoses: Etiologic
Classification
• Viral
• Bacterial
• Parasitic
• Mycotic
Zoonoses: Viral Examples
Colorado tick fever
Japanese encephalitis
Ebola
Monkeypox
Equine encephalitides
(WEE, EEE, VEE)
Hantaviruses
Nipah
Rabies
Hendra
Rift Valley fever
Herpesvirus B
West Nile virus
Influenza
Yellow fever
Zoonoses: Bacterial Examples
Anthrax
Plague
Brucellosis
Psittacosis
Campylobacteriosis
Q fever
Cat-scratch disease
Relapsing fevers
Leptospirosis
Salmonellosis
Listeriosis
Tularemia
Lyme disease
Yersiniosis
Zoonoses: Parasitic Examples
PROTOZOAL
HELMINTHIC
Trypanosomiasis
Baylisascariasis
Babesiosis
Cysticercosis
Cryptosporidiosis
Hydatidosis
Leishmaniasis
Schistosome dermatitis
Giardiasis
Trichinosis
Toxoplasmosis
Visceral larva migrans
and toxocariasis
Zoonoses: Mycotic Examples
Aspergillosis
Blastomycosis
Cryptococcosis
Dermatophytosis
Histoplasmosis
Sporotrichosis
Zoonoses: Animal Species
• Dogs & Cats
– Rabies
– Roundworm
– Ringworm
– Lyme Disease (dogs only)
– Cat Scratch Disease (cats only)
• Food Animals
– Salmonella
– E.coli
– Brucellosis
Zoonoses: Animal Species
• Birds:
– Psittacosis
– West Nile
– Cryptococcus
• Reptiles, Fish, &
Amphibians
– Salmonella
– Mycobacterium
• Wild Animals
– Hantavirus
– Plague
– Tularemia
Routes of Transmission
• Direct
– Droplet or Aerosol
– Oral
– Contact
• Indirect
– Foodborne
– Water-borne
– Fomite
– Vector-borne
– Environmental
Routes of Transmission
•
•
•
•
•
direct contact,
ingestion,
inhalation,
arthropod intermediates,
animal bites.
Dunne - CIDP
January 18, 2005
Zoonoses - Life Cycle
ORTHOZOONOSES
– May be perpetuated in nature by a
single vertebrate species
– E.g. rabies, brucellosis, anthrax
Zoonosis: Rabies Life Cycle
Virus
inoculation
(bite)
Salivary
gland
excretion
Dunne - CIDP
January 18, 2005
Zoonoses - Maintenance Cycle
CYCLOZOONOSES
– Requires more than one vertebrate
species but no invertebrate host
– Most are cestodiases (tapeworm
diseases)
• Taenia saginata and T. solium require
man to be one of vertebrate hosts
• Others, such as hydatidosis, man is
accidentally involved
Life Cycle:
Zoonoses - Life Cycle
METAZOONOSES
– Require both vertebrates and
invertebrates to complete transmission
– All arboviral infections
• West Nile virus, Saint Louis encephalitis
– Some bacterial diseases
• Plague, many rickettsia
– Some parasitic diseases
• Leishmaniasis, schistosomiasis
Zoonoses: Metazoonoses
• Invertebrate Host: Mosquitoes
• Vertebrate Host: Birds
• Incidental Hosts:
– HUMANS, horses, amphibians, other mammals
Risk Factors
• Companion Animal
– Dogs & roundworm
– Rats & Rat Bite Fever
• Occupational
– Animal control workers & rabies
– Wildlife biologists & hantavirus
• Foodborne
– Raw meat & E.coli
– Unpasteurized dairy & Listeria
Risk Factors
• Recreational Activities
– Camping & Lyme disease
• Farm Settings
– Sheep & Q-fever
– Cattle & Cryptosporidium
• Travel
– Malaysia & Nipha
– Australia & Hendra
Reportable Diseases of
Animals
• By veterinarian or other individual
• Reported to Health Services
– Plague
– Rabies
• Reportable to Dept Food and Agriculture
–
–
–
–
–
–
–
–
Anthrax
Brucellosis
Glanders
Listeriosis
Rabies in livestock
Venezuelan equine encephalomyelitis
West Nile
And more…
RABIES
Dunne - CIDP
January 18, 2005
Rabies Virus
• member of the Lyssavirus of the Rhabdoviridae.
• ssRNA enveloped virus, characteristic bullet-shaped appearance
with 6-7 nm spike projections.
• virion 130-240nm * 80nm
• -ve stranded RNA codes for 5 proteins; G, M, N, L, S
• Exceedingly wide range of hosts.
• There are 5 other members of Lyssavirus : Mokola, Lagosbat,
Duvenhage, EBL-1, and EBL-2.
• Duvenhage and EBL-2 have been associated with human rabies.
Rabies Virus
Structure of rabies virus (Source: CDC)
Rabies virus particles
DEFINITION
• Rabies is an acute, progressive
encephalomyelitis
• The case to fatality rate is the
highest of any infectious disease
• One of the oldest described diseases
• The leading viral zoonosis as
regards global public health
significance
Epidemiology
Rabies is a zoonosis which is prevalent in wildlife. The main
animals involved differs from continent to continent.
Europe
Middle East
Asia
Africa
N America
S America
fox, bats
wolf, dog
dog
dog, mongoose, antelope
foxes, skunks, raccoons,
insectivorous bats
dog, vampire bats
DISTRIBUTION
• Rabies is distributed on
all continents (with the
exception of Antarctica)
• Several areas are
considered ‘free’ of the
disease, including many
islands in Pacific
Oceania
• Globalization may
threaten the disease-free
status of many localities,
due to the introduction of
rabid animals
BURDEN
• More than ~55,000 human rabies deaths
per year
• Most occur in developing countries
• Millions of human exposures per year
• The domestic dog is the single most
important animal reservoir (>99%)
• Wildlife important, especially in
developed countries
RABIES PATHOGENESIS
•
•
•
•
Virus is transmitted via bite
Agents are highly neurotropic
Enter peripheral nerves
Centripetal travel by
retrograde flow in axoplasm of
nerves to CNS
• Replicate in brain
• Centrifugal flow to innervated
organs, including the portal of
exit, the salivary glands
• Viral excretion in saliva
Pathogenesis
• The commonest mode of transmission in man is by the bite of a
rabid animal, usually a dog. Rabies is an acute infection of the CNS
which is almost invariably fatal.
• Following inoculation, the virus replicates in the striated or
connective tissue at the site of inoculation and enters the peripheral
nerves through the neuromuscular junction.
• It then spreads to the CNS in the endoneurium of the Schwann cells.
• Terminally, there is widespread CNS involvement but few neurons
infected with the virus show structural abnormalities. The nature of
the profound disorder is still not understood.
CLINICAL STAGES
• Incubation Period (range =
~<7 days to >6 years;
average is ~4-6 weeks)
• Prodromal Phase (Nonspecific signs)
• Acute Neurological Phase
• Coma
• Death (recovery from
rabies?)
RABIES RECOVERY?
• Five historical human
case recoveries, after
vaccination, but before
illness onset
• Only one documented
unvaccinated human
survivor after clinical
presentation
RABIES DIAGNOSIS
• Based upon history of animal
exposure and typical
neurological clinical signs
• Postmortem demonstration of
viral antigen in CNS is gold
standard
• In humans, antemortem
detection of virus or viral
amplicons, antibodies, or
antigens (sera, csf, saliva,
nuchal biopsy)
Laboratory Diagnosis
• Histopathology - Negri bodies are pathognomonic of rabies. However,
Negri bodies are only present in 71% of cases.
• Rapid virus antigen detection - in recent years, virus antigen detection
by IF had become widely used. Corneal impressions or neck skin
biopsy are taken. The Direct Fluorescent Antibody test (DFA) is
commonly used.
• Virus cultivation - The most definitive means of diagnosis is by virus
cultivation from saliva and infected tissue. Cell cultures may be used
or more commonly, the specimen is inoculated intracerebrally into
infant mice. Because of the difficulties involved, this is rarely offered
by diagnostic laboratories.
• Serology - circulating antibodies appear slowly in the course of
infection but they are usually present by the time of onset of clinical
symptoms.
Diagnosis of Rabies
Negri Body in neuron cell
(source: CDC)
Positive DFA test (Source: CDC
PROPHYLAXIS
• Pre-exposure
Vaccination
• Postexposure
Prophylaxis (PEP)
Management and
Prevention
• Pre-exposure prophylaxis - Inactivated rabies vaccine may be
administered to persons at increased risk of being exposed to rabies e.g.
vets, animal handlers, laboratory workers etc.
• Post-exposure prophylaxis - In cases of animal bites, dogs and cats in a
rabies endemic area should be held for 10 days for observation. If signs
develop, they should be killed and their tissue.
• Wild animals are not observed but if captured, the animal should be
killed and examined. The essential components of postexposure
prophylaxis are the local treatment of wounds and active and passive
immunization.
• Once rabies is established, there is nothing much that could be done
except intensive supportive care. To date, only 2 persons with proven
rabies have survived.
Postexposure Prophylaxis
• Wound treatment - surgical debridement should be carried out.
Experimentally, the incidence of rabies in animals can be reduced by
local treatment alone.
• Passive immunization - human rabies immunoglobulin around the area
of the wound; to be supplemented with an i.m. dose to confer short
term protection.
• Active immunization - the human diploid cell vaccine is the best
preparation available. The vaccine is usually administered into the
deltoid region, and 5 doses are usually given.
• There is convincing evidence that combined treatment with rabies
immunoglobulin and active immunization is much more effective than
active immunization alone. Equine rabies immunoglobulin (ERIG) is
available in many countries and is considerably cheaper than HRIG.
RABIES BIOLOGICALS
• Rabies Vaccines (for pre- and PEP)
• Rabies immune globulin (only in PEP)
PRE-EXPOSURE
VACCINATION
• Vaccine given on days 0, 7, and 21 or 28
• Serology occurs every 6 months to 2 years (if
remaining at risk)
• If antibody titer not adequate, administer a single
booster dose
• If ever exposed, give a vaccine dose on days 0 and
3, regardless of titer
POSTEXPOSURE
PROPHYLAXIS
• Wash lesions well with
soap and water
(tetanus booster ad
hoc)
• Infiltrate rabies immune
globulin (20 IU/kg) into
and around the margin
of the bites
• Administer vaccine on
days 0,3,7,14, and 28
Control of Rabies
• Urban - canine rabies accounts for more than 99% of all human
rabies. Control measures against canine rabies include;
– stray dog control.
– Vaccination of dogs
– quarantine of imported animals
• Wildlife - this is much more difficult to control than canine
rabies. However, there are on-going trials in Europe where bait
containing rabies vaccine is given to foxes. Success had been
reported in Switzerland.
Arenaviruses
•
•
•
•
•
Lassa fever virus particles budding
from the surface of an infected cell.
(Source: CDC)
•
Enveloped ssRNA viruses
virions 80-150nm in diameter
genome consists of 2 pieces of
ambisense ssRNA.
7-8 nm spikes protrude from the
envelope.
host cell ribosomes are usually seen
inside the outer membrane but play
no part in replication.
Members of arenaviruses include
Lassa fever, Junin and Macupo
viruses.
Lassa Fever

Found predominantly in West Africa, in
particular Nigeria, Sierra Leone and
Liberia.

The natural reservoir is multimammate rat
(Mastomys)

Man may get infected through contact with
infected urine and faeces.

Man to man transmission can occur
through infected bodily fluids and Lassa
fever had caused well-documented
nosocomial outbreaks.
Mastomys
Clinical Manifestations
• Incubation period of 3-5 days.
• Insidious onset of non-specific symptoms such as fever, malaise,
myalgia and a sore throat.
• Typical patchy or ulcerative pharyngeal lesions may be seen.
• Severe cases may develop the following:
–
–
–
–
–
Myocarditis
Pneumonia
Encephalopathy
Haemorrhagic manifestations
Shock
• The reported mortality rate for hospitalized cases of Lassa fever is 25%.
It carries a higher mortality in pregnant women.
Laboratory Diagnosis
Lassa fever virus is a Group 4 Pathogen. Laboratory diagnosis should only
be carried out in specialized centers.
– Detection of Virus Antigen - the presence of viral antigen in sera can be
detected by EIA. The presence of viral antigen precedes that of IgM.
– Serology - IgM is detected by EIA. Using a combination of antigen and
IgM antibody tests, it was shown that virtually all Lassa virus
infections can be diagnosed early.
– Virus Isolation - virus may be cultured from blood, urine and throat
washings. Rarely carried out because of safety concerns.
– RT-PCR - being used experimentally.
Management and
Prevention
• Good supportive care is essential.
• Ribavirin - had been shown to be effective against Lassa fever with a 2
to 3 fold decrease in mortality in high risk Lassa fever patients. Must
be given early in the illness.
• Hyperimmune serum - the effects of hyperimmune serum is still
uncertain although dramatic results have been reported in anecdotal
case reports.
• Postexposure Prophylaxis - There is no established safe prophylaxis.
Various combinations of hyperimmune immunoglobulin and/or oral
ribavirin may be used.
• There is no vaccine available, prevention of the disease depends on
rodent control.
Hantaviruses
•
•
•
•
•
Forms a separate genus in the
Bunyavirus family.
Unlike under bunyaviridae, its
transmission does not involve an
arthropod vector.
Enveloped ssRNA virus.
Virions 98nm in diameter with a
characteristic square grid-like
structure.
Genome consists of three RNA
segments: L, M, and S.
History
• Haemorrhagic Fever with Renal Syndrome (HFRS: later
renamed hantavirus disease) first came to the attention of the
West during the Korean war when over 3000 UN troops were
afflicted.
• It transpired that the disease was not new and had been
described by the Chinese 1000 years earlier.
• In 1974, the causative was isolated from the Korean Stripped
field mice and was called Hantaan virus.
• In 1995, a new disease entity called hantavirus pulmonary
syndrome was described in the “four corners” region of the U.S.
Some Subtypes of hantaviruses
associated with human disease
•
Hantaan, Porrogia and related viruses - This group is found in China,
Eastern USSR, and some parts of S. Europe. It is responsible for the severe
classical type of hantavirus disease. It is carried by stripped field mice.
(Apodemus agrarius)
•
Seoul type - associated with moderate hantavirus disease. It is carried by
rats and have a worldwide distribution. It has been identified in China,
Japan, Western USSR, USA and S.America.
•
Puumala type - mainly found in Scandinavian countries, France, UK and
the Western USSR. It is carried by bank voles (Clethrionomys glareolus)
and causes mild hantavirus disease (nephropathia epidemica).
•
Sin Nombre - found in many parts of the US, Canada and Mexico. Carried
by the Deer Mouse (Peromyscus maniculatus) and causes hantavirus
pulmonary syndrome.
Rodent Carriers of
Hantaviruses
Stripped field mouse (Apodemus agrarius)
Bank vole (Clethrionomys glareolus)
Deer Mouse (Peromyscus maniculatus)
Rat (Rattus)
Clinical Features of Hantavirus
Disease
• The multisystem pathology of HVD is characterized by damage to
capillaries and small vessel walls, resulting in vasodilation and
congestion with hemorrhages.
• Classically, hantavirus disease consists of 5 distinct phases. These
phases may be blurred in moderate or mild cases.
– Febrile phase - abrupt onset of a severe flu-like illness with a
erythematous rash after an incubation period of 2-3 days.
– Hypotensive phase - begins at day 5 of illness
– Oliguric phase - begins at day 9 of illness. The patient may develop acute
renal failure and shock. Haemorrhages are usually confined to petechiae.
The majority of deaths occur during the hypotensive and oliguric phases
– Diuretic phase - this occurs between days 12-14 .
– Convalescent phase - this may require up to 4 months.
Comparative Clinical Features of
Recognized Hantavirus Disease (HVD)
Nephropathia
Epidermica
Virus type
Far Eastern
HVD
Rat-bourne
HVD
Balkan
HVD
Puumala
Hantaan
Seoul
Porogia
1-2
2-4
1-3
2-4
Yes
Blurred
Yes
1-2
4
1-2
4
0
0-1
1-3
0-1
Haemorrhagic phenomenon
0-1
1-4
1-2
1-4
Mortality
<1%
5-10%
Overall Severity
Multiphasic Disease
Renal Abnormalities
Hepatic abnormalities
Score = 0 to 4
occasionally
1%
5-35%
Hantavirus Pulmonary Syndrome
(HPS)
• More than 250 cases of HPS have been reported throughout North
and South America with a mortality rate of 50%
• In common with classical HVD, HPS has a similar febrile phase.
• However, the damage to the capillaries occur predominantly in the
lungs rather than the kidney.
• Shock and cardiac complications may lead to death.
• The majority of HPS cases are caused by the Sin Nombre virus.
The other cases are associated with a variety of other hantaviruses
e.g. New York and Black Creek Canal viruses.
Diagnosis
• Serological diagnosis - a variety of tests including IF, HAI, SRH, ELISAs
have been developed for the diagnosis of HVD and HPS.
•
Direct detection of antigen - this appears to be more sensitive than
serology tests in the early diagnosis of the disease. The virus antigen can
be demonstrated in the blood or urine.
• RT-PCR - found to of great use in diagnosing hantavirus pulmonary
syndrome.
• Virus isolation - isolation of the virus from urine is successful early in
hantavirus disease. Isolation of the virus from the blood is less consistent.
Sin Nombre virus has never been isolated from patients with HPS.
• Immunohistochemistry - useful in diagnosing HPS.
68
National Statutory Notifiable Communicable
Diseases
• Group A: Plague, Cholera
• Group B: SARS, AIDS, Viral hepatitis, Poliomyelitis, HPAI,
Measles, HFRS, Rabies, Japanese encephalitis, Dengue fever,
Anthrax, Bacillary & amebic dysentery, TB, Typhoid
fever/Paratyphoid fever, Meningococcal Meningitis, Pertussis,
Diphtheria, Neonatal Tetanus, Scarlet fever, Brucellosis,
Gonorrhea, Syphilis, Leptospirosis, Schistosomiasis, Malaria
• Group C: Influenza, Mumps, Rubella, Acute hemorrhagic
Conjunctivitis, Leprosy, Epidemic typhus/Endemic typhus, kalaazar, Echinococcosis, Filariasis, Infectious diarrhea
69
Animal Health - Human Health Collaboration • “Effective control of zoonotic disease relies on
active involvement of both veterinary and
human health services.”
• “This dual involvement needs to take place at
every stage, from research, organizing
funding, planning, surveillance, creating
public awareness, to implementing the actual
control activities.”
TULAREMIA
Dunne - CIDP
January 18, 2005
Tularemi
• Francisella tularensis is the causative
agent of tularemia (a reportable disease)
• F. tularensis is a small, Gram-negative,
nonmotile, encapsulated, pleomorphic
coccobacillus (short rod).
• It is a facultative intracellular parasite that
grows poorly or not at all on most lab
media and requires a special blood agar
Dunne - CIDP
January 18, 2005
• Human commonly acquires tularemia via
• the insect bites (ticks primarily, but also
deer flies, mites, blackflies, or
mosquitoes) or
• by handling infected animal tissues.
Human disease (rabbit or deer fly fever)
is characterized by a focal ulcer at the
site of entry of the organisms and
enlargement of the regional lymph nodes.
Dunne - CIDP
January 18, 2005
• As few as10-50 bacilli will cause
disease in humans if inhaled or
introduced intradermally, whereas a
very large inoculum (~108 organisms)
is required for the oral route of
infection.
Dunne - CIDP
January 18, 2005
• Incubation period is 3-10 days.
• A small skin papule usually develops
at the site of entry.
• Ulceration occurs together with fever,
chills, malaise, fatigue, and usually
lymphadenopathy.
Dunne - CIDP
January 18, 2005
• Bacteremia usually occurs and the
bacilli then grow intracellularly in the
reticuloendothelial system.
• Dissemination of the organisms
through the bloodstream permits
focal lesions to develop in numerous
organs
Dunne - CIDP
January 18, 2005
Epidemiology
• Summer peak related to ticks
– 90% pediatric cases
• Winter peak related to trapping and
hunting of rabbits
Photo courtesy of National Archives
Tularemia
Geographic distribution
Clinical Manifestations
• Six classic froms;
– Ulceroglandular
– Glandular
– Oculoglandular
– Pharyngeal
– Typhoidal
– Pneumonie
Diagnosis of tularemia
• Clinical suspicion
• Organism rarely seen on Gram stained
smears
• Direct fluorescent antibody staining of
smears,tissues
• Antigen detection in urine
• PCR
• Most common way of diagnosis serology
(tube agg, microagg, hemagg, ELISA)
Treatment
• First choice is streptomycin
• Gentamycin alternative
YERSINIA
Dunne - CIDP
January 18, 2005
Yersinia pestis
• Plague, disease of antiquity
• Three catastrophic pandemics
• Latest pandemic began in China in the
1860s.
• Recently resurged in sub-Saharan Africa.
• Aerosol weapon during the Cold War
(catagory A biologic agent).
Yersinia pestis
• Gram negative, bipolar-staining bacillus
• Grows aerobically on most culture media,
more slowly and optimally at 28°C
• Non-motile and non-spore forming
• Not ferment lactose
• Citrate, urease and indole negative
Transmission of plague
• Plague is primarily an infection of animals
• Transmitted by flea bites
• Domestic rats are the most dangerous
reservoirs
• Most efficient vector to humans is oriental
rat flea
Clinical manifestations
• Pharingeal
• Fever, painful lymphadenopathy
(bubo)
• Fever, hypotension comp. of
inflammatory response syndrome
• Cough, hemoptysis with /without
bubo
• Painful, inflamed pharinx, local
lymphadenopathy
• Meningitis
• Fever, nuchal rigidity with bubo
• Bubonic
• Septicemic
• Pneumonic
Diagnosis
• WBC elevated (10.000-20.000)
predominance of neutrophils
• Clinical specimens (blood, bubo aspirate)
• Chest x-rays
• Serologic test (passive hemagg test,
ELISA,), PCR
Treatment
•
•
•
•
Streptomycin drug of choice
Gentamicin
Tetracycline
Chloramphenicol
BRUCELLOSIS
Dunne - CIDP
January 18, 2005
• Brucella are Gram-negative,
nonmotile, coccobacilli. They are
strict aerobes that grow very slowly
(fastidious) on blood agar. In the
host, they live as facultative
intracellular pathogens.
Dunne - CIDP
January 18, 2005
• Brucellosis is primarily a disease of animals
and it affects organs rich in the sugar
erythritol (breast, uterus, epididymis, etc.).
The organism localizes in these animal
organs and causes infertility, sterility, mastitis,
abortion, or resides as carriage. Humans in
close contact with infected animals
(slaughterhouse workers, veterinarians,
farmers, dairy workers) are at risk of
developing undulant fever.
Dunne - CIDP
January 18, 2005
PATHOGENS
• Four different species of Brucella
are known to infect humans:
• B. abortus (cattle),
• B. suis (swine),
• B. melitensis (goats/sheep) and
• B. canis (dogs).
Dunne - CIDP
January 18, 2005
• B. abortus and B. canis cause a mild
suppurative febrile infection whereas B.
suis causes a more severe suppurative
infection which can lead to destruction
of the lymphoreticular organs and
kidney.
• B. melitensis is the cause of most
severe and prolonged recurring
disease.
Dunne - CIDP
January 18, 2005
PATHOGENESIS
• The bacteria enter the human host
through the mucous membranes of
the oropharynx (ingestion/inhalation
routes), through abraded skin, or
through the conjunctiva.
• Usually infection occurs by direct
contact with infected material,
although it may also occur by
ingestion of milk or milk products.
Dunne - CIDP
January 18, 2005
TREATMENT
• Prolonged treatment with Tetracyclin
combined with Rifampin that penetrates
cells, is effective.
• Control measures include animal
vaccination and avoidance of infected
material (e.g., unpasteurized dairy
products).
Dunne - CIDP
January 18, 2005
• The symptoms in brucellosis are
due to the presence of the organism
and appear 2-4 weeks (sometimes
up to 2 months) after exposure.
Dunne - CIDP
January 18, 2005
• Diagnosis is based on prolonged (at least a week)
presence of undulant fever, myalgia, arthralgia and the
history of exposure (contact with animals or consumption
of unprocessed material from infected animals).
Definitive diagnosis can be made by culturing blood
samples on blood-enriched media. The (fastidious)
organisms grow very slowly (4-6 weeks in blood culture).
B. abortus but not other Brucella grow better in 5% CO2
atmosphere (microaerophilic). On blood agar, they
produce white glistening colonies.
• Specific antibodies can be used to further confirm the
diagnosis
Dunne - CIDP
January 18, 2005
TTUS 2013
• Aşağıdaki etkenlerden hangisi,
insana artropod ısırığı ile bulaşır?
A) Listeria monocytogenes
B) Nocardia brasiliensis
C) Francisella tularensis
D) Chlamydia psittaci
E) Campylobacter jejuni
Dunne - CIDP
January 18, 2005
TTUS 2013
• Aşağıdaki etkenlerden hangisi,
insana artropod ısırığı ile bulaşır?
A) Listeria monocytogenes
B) Nocardia brasiliensis
C) Francisella tularensis
D) Chlamydia psittaci
E) Campylobacter jejuni
Dunne - CIDP
January 18, 2005
QUESTION