Zoonosis

Zoonosis D-r Mitova MU-Sofia

Modes of Disease Transmission

Zoonoses From the Greek: Zoon: Animal Noson: Disease Diseases and infections which are naturally transmitted between vertebrate animals and humans - WHO 1959

Zoonoses
> 250 zoonotic diseases

Zoonoses: Common Diseases
Frequency – (CDC, 2003)
Salmonella 39,919
Lyme disease 18,991
West Nile (CNS) 2,862
Trichinosis 4

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

Zoonoses: Etiologic Classification
Viral
Bacterial
Parasitic
Mycotic

Zoonoses: Viral Examples Yellow fever Influenza West Nile virus* Herpesvirus B Rift Valley fever Hendra* Rabies* Hantaviruses Nipah* Equine encephalitides (WEE, EEE, VEE) Monkeypox* Ebola Japanese encephalitis Colorado tick fever

Zoonoses: Bacterial Examples Yersiniosis Lyme disease* Tularemia* Listeriosis* Salmonellosis* Leptospirosis* Relapsing fevers Cat-scratch disease* Q fever* Campylobacteriosis* Psittacosis* Brucellosis* Plague* Anthrax*

Zoonoses: Animal Species
Dogs & Cats
Rabies
Lyme Disease (dogs only)
Food Animals
Salmonella
E.coli
Brucellosis

Zoonoses: Animal Species
Birds:
Psittacosis
West Nile
Wild Animals
Hantavirus
Plague
Tularemia

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.

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.

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.

Routes of Transmission
Direct
Droplet or Aerosol
Oral
Contact
Indirect
Foodborne
Water-borne
Fomite
Vector-borne
Environmental

Risk Factors
Companion Animal
Dogs & roundworm
Rats & Rat Bite Fever
Occupational
Animal control workers & rabies
Wildlife biologists & hantavirus
Foodborne
E.coli

Risk Factors
Recreational Activities
Camping & Lyme disease
Farm Settings
Sheep & Q-fever
Travel
Maylasia & Nipha
Australia & Hendra

Yersinia pestis
Family Enterobacteriaceae
Gram negative coccobacillus (pleomorphic)
Aerobic, Facultatively anaerobic
Facultative intracellular pathogen
Survival
Briefly in soil
Soft tissue ~1 week
Frozen - years

History
Outbreaks
Justinian’s pandemic: 540-590
Black Death pandemic: 1346~1400
Great Plague of London: 1665
Hawaii, 1899
San Francisco, 1900

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)

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

Flea Vectors
Can live off host for months
Many species can transmit

Plague Epidemiology in Nature
Sylvatic (wild)
Urban (domestic)
Reservoirs
Rock squirrels
Ground squirrels
Prairie dogs
Mice
Voles
Others

Sylvatic Plague
Enzootic
Plague maintained at steady level in rodent populations
Low death rates
Mice, voles

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

Robert B. Crave. Plague. Infectious Diseases, 5 th ed. J.B. Lippincott Co. 1994.

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

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

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

Laboratory Confirmation
Acceptable specimens
Material from infected bubo
Blood specimen (Series taken 10-30 minutes apart)
Bronchial or Tracheal Wash
Sputum (Not the best)

Laboratory Diagnostic Tests PLAGUE Colonial Morphology on SBA at 72 hrs Gram Stain

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

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.

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.

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.

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.

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

Transmission
Aerosol
Parturient fluids
10 9 bacteria per gram of placenta
Urine, feces, milk
Direct contact
Fomites
Ingestion
Arthropods (ticks)

Transmission
Person-to-person (rare)
Transplacental (congenital)
Blood transfusions
Intradermal inoculation
Bone marrow transplants
Possibly sexually transmitted

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%

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

Diagnosis
Serology (rise in titer)
IFA, CF, ELISA, microagglutination
DNA detection methods
PCR
Isolation of organism
Risk to laboratory personnel
Rarely done

Treatment
Treatment
Doxycycline
Chronic disease – long course
2-3 years of medication
Immunity
Long lasting (possibly lifelong)

Prevention and Control
Pasteurization
Vaccination
Human and animal
Eradication not practical
Too many reservoirs
Constant exposure
Stability of agent in environment

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.

Rabies Virus Structure of rabies virus (Source: CDC) Rabies virus particles

Epidemiology
Rabies is a zoonosis which is prevalent in wildlife. The main animals involved differs from continent to continent.

Europe fox, bats
Middle East wolf, dog
Asia dog
Africa dog, mongoose, antelope
N America foxes, skunks, raccoons, insectivorous bats
S America dog, vampire bats

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.

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.

Negri Body in neuron cell (source: CDC) Positive DFA test (Source: CDC Diagnosis of Rabies

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
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)

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 RNA 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)

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.

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.

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.

 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. 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. 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. 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. Rodenticides

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.

 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 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. 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 Rodenticides

Zoonosis

by Jasmine John

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