Zoonosis
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Modes of Disease Transmission
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Zoonoses
From the Greek:
Zoon:
Animal
Noson: Disease
Diseases and infections which are
naturally transmitted between
vertebrate animals and humans
- WHO 1959
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Zoonoses
> 250 zoonotic diseases
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Zoonoses: Common Diseases
Frequency – (CDC, 2003)
Salmonella
39,919
Lyme disease
18,991
West Nile (CNS)
2,862
Trichinosis
4
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Zoonoses
Spectrum of Disease Severity
Death = rabies
Severe illness = plague
Chronic illness = Q-fever
Mild illness = psittacosis
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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
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Zoonoses: Etiologic Classification
Viral
Bacterial
Parasitic
Mycotic
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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
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Zoonoses: Bacterial Examples
Anthrax*
Plague*
Brucellosis*
Psittacosis*
Campylobacteriosis*
Q fever*
Cat-scratch disease*
Relapsing fevers
Leptospirosis*
Salmonellosis*
Listeriosis*
Tularemia*
Lyme disease*
Yersiniosis
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Zoonoses: Animal Species
Dogs & Cats
Rabies
Lyme Disease (dogs only)
Food Animals
Salmonella
E.coli
Brucellosis
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Zoonoses: Animal Species
Birds:
Psittacosis
West Nile
Wild Animals
Hantavirus
Plague
Tularemia
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The Rat
The best-known rat species are the Black Rat Rattus
rattus and the Brown Rat R. norvegicus. The group is
generally known as the Old World rats or true rats,
and originated in Asia. Rats are bigger than most of
their relatives, the Old World mice, but seldom weigh
over 500 grams (1 lb) in the wild. The common term
"rat" is also used in the names of other small
mammals which are not true rats. Examples include
the North American pack rats, a number of species
loosely called kangaroo rats, and a number of others.
Other rats such as the Bandicoot rat Bandicota
bengalensis are murine rodents related to the true
rats, but are not members of the genus Rattus.
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Roof Rat
Order Rodentia : Family Muridae : Rattus
rattus (Linnaeus)
Description. A blackish (or brownish),
medium-sized, slender rat with long,
naked, scaly tail; tail usually longer than
head and body but not always so.
External measurements average: total
length, 370 mm; tail, 190 mm; hind
foot, 36 mm. Weight, up to 200 g.
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Norway Rat
Order Rodentia : Family Muridae : Rattus
norvegicus (Berkenhout)
Description. Similar to the roof rat but
larger and chunkier; tail shorter than
length of head and body. External
measurements average: total length,
440 mm; tail, 205 mm; hind foot, 46
mm. Weight, 400-500 g.
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Routes of Transmission
Direct
Droplet or Aerosol
Oral
Contact
Indirect
Foodborne
Water-borne
Fomite
Vector-borne
Environmental
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Risk Factors
Companion Animal
Dogs & roundworm
Rats & Rat Bite Fever
Occupational
Animal control workers & rabies
Wildlife biologists & hantavirus
Foodborne
E.coli
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Risk Factors
Recreational Activities
Camping & Lyme disease
Farm Settings
Sheep & Q-fever
Travel
Maylasia & Nipha
Australia & Hendra
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Yersinia pestis
Family Enterobacteriaceae
Gram negative coccobacillus (pleomorphic)
Aerobic, Facultatively anaerobic
Facultative intracellular pathogen
Survival
Briefly in soil
Soft tissue ~1 week
Frozen - years
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History
Outbreaks
Justinian’s pandemic: 540-590
Black Death pandemic: 1346~1400
Great Plague of London: 1665
Hawaii, 1899
San Francisco, 1900
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Black Death Pandemic
Sudden appearance in Europe 1347
Rattus rattus and Xenopsylla cheopis
Quarantine
Sporadic outbreaks throughout 14th
century
17-55 million perished (1/3 of population)
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Transmission to Humans
Flea bite ~78%
Especially those associated with ground
squirrels
Direct animal contact ~20%
Tissues, body fluids, scratches, bites
• Y. pestis enters through break in skin
Aerosol (ie, cough) ~2%
Cats
Human cases, April-November
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Flea Vectors
Can live off host for months
Many species can transmit
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Plague Epidemiology in Nature
Sylvatic (wild)
Urban (domestic)
Reservoirs
Rock squirrels
Ground squirrels
Prairie dogs
Mice
Voles
Others
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Sylvatic Plague
Enzootic
Plague maintained at steady level in rodent
populations
Low death rates
Mice, voles
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Sylvatic Plague
Epizootic
Large die-offs, fleas
change hosts
Amplifying hosts: prairie
dogs, ground squirrels,
rock squirrels, woodrats,
chipmunks
Expansion into human
occupied areas
Greatest threat to
humans
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Robert B. Crave. Plague. Infectious Diseases, 5th ed. J.B.
Lippincott Co. 1994.
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Urban Plague
Infected fleas or rodents move to urban
area
Interface areas around homes
Commensal (domestic) rodents
Roof rat, Norway rat
Rat fleas may feed on humans
Poverty, filth, homelessness
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Human Disease
Bubonic:
Cutaneous infection
Swollen, tender lymph
glands (buboes)
Fever, chills, headache,
exhaustion
Septicemic
Multiplication in bloodstream
Fever, chills, prostration,
abdominal pain, shock,
bleeding into skin
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Human Disease
Pneumonic:
1 – 4 day incubation period
Infection of the lungs
High fever, chills, cough, difficulty breathing,
bloody sputum
Most likely for BT (may also see
gastrointestinal manifestations)
100% fatal if not treated early
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Laboratory Confirmation
Acceptable specimens
Material from infected bubo
Blood specimen (Series taken 10-30 minutes
apart)
Bronchial or Tracheal Wash
Sputum (Not the best)
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Laboratory Diagnostic Tests
PLAGUE
Colonial Morphology
on SBA at 72 hrs
Gram Stain
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Plague Treatment and Prophylaxis
Without treatment: Death 2-6 days after
exposure
Treatment is effective if begun early
Symptomatic Exposed (cough or fever)
Streptomycin or Gentamicin
Doxycycline or Tetracycline
Ciprofloxacin
Post-exposure Prophylaxis
Doxycycline or Ciprofloxacin (7 days)
Fever/Cough watch
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Anthrax
Anthrax is primarily a disease of herbivorous
mammals, although other mammals and
some birds have been known to contract it.
Until the introduction and widespread use
of effective veterinary vaccines, it was a
major cause of fatal disease in cattle,
sheep, goats, camels, horses, and pigs
throughout the world.
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Anthrax
Humans generally acquire the disease
directly or indirectly from infected animals,
or occupational exposure to infected or
contaminated animal products. Control in
livestock is therefore the key to reduced
incidence. The disease is generally
regarded as being non-contagious. Records
of person-to-person spread exist, but are
rare.
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Leptospirosis
Leptospirosis is an infection in rodents and
other wild and domesticated species. Rodents
are implicated most often in human cases.
The infection in man is contracted through
skin abrasions and the mucosa of the nose,
mouth and eyes. Exposure through water
contaminated by urine from infected animals
is the most common route of infection.
Human-to-human transmission is rare.
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Leptospirosis
Outdoor and agricultural workers (rice-paddy
and sugarcane workers for example) are
particularly at risk but it is also a recreational
hazard to those who swim or wade in
contaminated waters. In endemic areas the
number of leptospirosis cases may peak
during the rainy season and even may reach
epidemic proportions in case of flooding
because the floods cause rodents to move
into the city.
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Q-fever
Coxiella burnetii
Rickettsial agent
Obligate intracellular parasite
Stable and resistant
Killed by pasteurization
Two antigenic phases
• Phase 1: virulent
• Phase 2: less pathogenic
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Transmission
Aerosol
Parturient fluids
• 109 bacteria
per gram of placenta
Urine, feces, milk
Direct contact
Fomites
Ingestion
Arthropods (ticks)
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Transmission
Person-to-person (rare)
Transplacental (congenital)
Blood transfusions
Intradermal inoculation
Bone marrow transplants
Possibly sexually transmitted
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Acute Infection
Flu-like, self limiting
Atypical pneumonia (30-50%)
Non-productive cough, chest pain
Acute respiratory distress possible
Hepatitis
Skin rash (10%)
Other signs (< 1%)
Myocarditis, pericarditis, meningoencephalitis
Death: 1-2%
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Prognosis
Overall case-fatality rate <1 - 2.4%
50% cases self-limiting
Only 2% develop severe disease
Active chronic disease
Usually fatal if left untreated
Fatality for endocarditis: 35-55%
50-60% need valve replacement
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Diagnosis
Serology (rise in titer)
IFA, CF, ELISA, microagglutination
DNA detection methods
PCR
Isolation of organism
Risk to laboratory personnel
Rarely done
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Treatment
Treatment
Doxycycline
Chronic disease – long course
• 2-3 years of medication
Immunity
Long lasting (possibly lifelong)
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Prevention and Control
Pasteurization
Vaccination
Human and animal
Eradication not practical
Too many reservoirs
Constant exposure
Stability of agent in environment
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Rabies Virus
member of the Lyassavirus of the Rhabdoviridae.
ssRNA enveloped virus, characteristic bullet-shaped appearance
with 6-7 nm spike projections.
virion 130-240nm * 80nm
5 proteins; G, M, N, L, S
Exceedingly wide range of hosts.
There are 5 other members of Lyassavirus : Mokola, Lagosbat,
Duvenhage, EBL-1, and EBL-2.
Duvenhage and EBL-2 have been associated with human rabies.
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Rabies Virus
Structure of rabies virus (Source: CDC)
Rabies virus particles
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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
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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.
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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.
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Diagnosis of Rabies
Negri Body in neuron cell
(source: CDC)
Positive DFA test (Source: CDC
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.
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Arenaviruses
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 virus particles budding
from the surface of an infected cell.
(Source: CDC)
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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.
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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.
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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.
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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.
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Hantaviruses
Forms a separate genus in the
Bunyavirus family.
Unlike under bunyaviridae, its
transmission does not involve an
arthropod vector.
Enveloped RNA virus.
Virions 98nm in diameter with a
characteristic square grid-like
structure.
Genome consists of three RNA
segments: L, M, and S.
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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.
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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.
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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.
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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
occasionally
1%
5-35%
Score = 0 to 4
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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.
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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.
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Treatment and Prevention
Treatment of HVD and HPS depends mainly on supportive
measures.
Ribavirin - reported to be useful if given early in the course of
hantavirus disease. Its efficacy is uncertain in hantavirus
pulmonary syndrome.
Vaccination - an inactivated vaccine is being tried out in China.
Other candidate vaccines are being prepared.
Rodent Control - control measures should be aimed at reducing
contact between humans and rodents.
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Rodenticides
Rodenticides may be classified in several ways but the most
medically useful of classifying them is by toxicity.
Highly toxic rodenticides
Highly toxic rodenticides are those substances with
a single dose LD50 of less than 50mg/kg body
weight. This group includes thallium, sodium
monofluoroacetate, strychnine, zinc phosphide,
yellow phosphorus and arsenic. Some of these
compounds have largely been abandoned because
of serious human toxicity.
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Rodenticides
Thallium
Thallium is an odourless; tasteless compound that can be absorbed
through unbroken skin and can cause death secondarily. There is no
known effectiveness antidote for thallium. In sublethal doses, thallium
can cause complete loss of hair, paresthesias, nausea, vomiting and
abdominal pain, pulmonary oedema and bronchopneumonia.
·
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Rodenticides
· Sodium monofluoroacetate
Sodium monofluoroacetate is a white, odourless, tasteless, water-soluble salt that
looks like flour or baking soda. Unlike thallium, sodium monofluoroacetate cannot
be absorbed through unbroken skin. However, it is toxic when ingested, inhaled in
dust or absorbed through open wounds.
Toxic effects in humans, extrapolated from observed effects in rhesus monkeys,
might be nausea and apprehension followed by cardiac arrhythmias, seizures and
coma. Death may result from ventricular tachycardia and fibrillation or respiratory
failure secondary to pulmonary oedema or bronchopneumonia.
· Strychnine
Strychnine is a central nervous system stimulant that causes painful recurrent motor
seizures. It is rapidly absorbed from the gastrointesstinal tract and nasal mucosa but
not from the skin. Symptoms include nausea and vomiting, diaphoresis, blurred
vision and severe symmetric extensor muscle spasms during which patients are
conscious.
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Rodenticides
· Zinc phosphide
Zinc phosphide is another highly toxic rodenticide in which its colour,
"rotten fish" odour and taste make it unattractive to other animals but
attractive to other animals but attractive to rats. Usually mixed with a
tartar emetic, it nevertheless is highly toxic because it releases phosphine
gas on contact with water or weak acids.
Poisoned patients manifest hypotension, dyspnea, pulmonary oedema,
circulatory collapse, vomiting, cardiac arrhythmias, convulsions and
coma, renal damage, leukopenia and death in four days to two weeks.
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Rodenticides
Yellow phosphorus
Yellow phosphorus is highly poisonous compares with the relatively non- toxic red
phosphorus. When used as a rodenticide, yellow phosphorus is usually mixed with
molasses or peanut butter and spread on bread as bait for rodents or roaches. For
obvious reasons, it is occasionally ingested by children.
Yellow phosphorus is most toxic to the gastrointestinal tract and liver. Ingestion is
usually followed by vomiting which is said to be luminescent and have a garlicky
odour. Delirium, coma and death from cardiovascular collapse may ensue.
· Arsenic
Arsenic is a white, crystalline powder that causes dysphagia, muscle cramps,
convulsions, vomiting and bloody diarrhoea. Death can occur due to circulatory failure.
·
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Low toxicity rodenticides
Low toxicity rodenticides are those with LD50 between 500 and 5,000
mg/kg body weight and include red squill, norbomide and
anticoagulant, warfarin-type rodenticides, which are the most
commonly used rodenticides today.
· Red squill
Red squill contains several compounds with chemical and
pharmacological properties similar to those of digitalis glycosides.
Because of its emetic properties, poor gastrointestinal absorption and
decreased potency (compared to that of digitalis), red squill has seldom
been associated with human toxicity.
· Norbomide
Norbomide is an irreversible smooth muscle constrictor. It causes
widespread ischaemic necrosis and death in rats but does not appear to
affect other animals or humans, presumably due to the presence of a
specific smooth muscle norbomide
receptor found only in rats.
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Rodenticides
·
Anticoagulant
Anticoagulant rodenticides belong to a group that exerts a blood-thinning
effect. It has been used for many decades and are readily available as
over- the counter preparations.
Technically, these may be divided into two types: hydroxiycoumarin
compounds are made up of warfarin, difenacoum, bromadiolone and
brodifacoum while the indandiones cover a wide range of chemicals
including diphacinone, pindone and chlorphacinone. Aside from
warfarin, the others are said to be longer-acting. They produce a more
potent and prolonged anticoagulant effect and they are often referred to
as superwarfarins
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Rodenticides
Haemorrhage is the most frequent encountered complication from
anticoagulant poisoning. The effect seen in cases of acute ingestion,
however, depends very much on whether warfarin or superwarfarin
rodenticides have been ingested. A one-time ingestion of warfarin
usually does not lead to any bleeding problems. Otherwise, ingestion of
warfarin rodenticides has to be done repeatedly over a periods of days
before bleeding can occur.
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Rodenticides
Warfarin poisoning can cause spontaneous bleeding, usually from
the nose, gums as well as the gastrointestinal and urinary tracts.
Haemorrhage into the skin and brain can also occur, throuh this is
less common. Ingestion of superwarfarin, on the other hand, can
produce a prolonged coagulopathy in humans even with a single
ingestion. This is thought to be associated with the firmer binding
capability of superwarfarins to the lipophilic sites of the liver
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