Contact zoonotic disease

Dr. Wahid Elsaidy
Assistant lecturer of public health and
community medicine
11/24/2016 Dr.Wahid Elsaidy 2

( From Latin: rabies, "madness")
‫السعار‬ ‫الكلب‬ ‫داء‬
Definition
Acute viral zoonosis affecting domestic and wild
animals, transmitted through the bit of rabid
animal
11/24/2016 Dr.Wahid Elsaidy

Occurrence
In Egypt estimated that 200000 animal bites occur
each year
Prepathogenic period
Agent : rabies virus is the type species of the
Lyssavirus genus ,in the family Rhabdoviridae,
order Mononegavirales. RNA
Source of infection: Carnivorous animals
(dogs,foxes,raccoons,bats)
Exit : saliva of the infected animals

Mode of transmission:
1- bite of rabid animals
2- licks on skin(abraded) or
mucosa (abraded or non abraded)
3- aerosol of the virus that can
be present in caves where bats roots

Pathogenic period :
10 days to one year commonly (1-3) months
‫على‬ ‫وتعتمد‬
 The bits : number , severity , distance from the brain
 The virus : amount , strain
 The skin : bare or covered with clothes

Clinical picture
 The period between infection and the first flu-like
symptoms is normally two to twelve weeks, but can
be as long as one year.
 the symptoms expand to slight or partial paralysis,
cerebral dysfunction, anxiety, insomnia, confusion,
agitation, abnormal behavior, paranoia, terror,
hallucinations, progressing to delirium.

 The production of large quantities of saliva and tears
coupled with an inability to speak or swallow are
typical during the later stages of the disease; this can
result in hydrophobia, in which the patient has
difficulty swallowing because the throat and jaw
become slowly paralyzed, shows panic when
presented with liquids to drink, and cannot quench
his or her thirst.
 Death almost invariably results two to ten days after
first symptoms.

Diagnosis
 PCR or viral culture
 It is also possible to make the diagnosis from saliva,
urine and cerebrospinal fluid samples, but this is not
as sensitive.
 Cerebral inclusion bodies called Negri bodies
are 100% diagnostic for rabies infection, but
are found in only about 80% of cases. If
possible, the animal from which the bite was
received should also be examined for rabies.

Prevention
A. Measures of animals
 Dogs should be licensed and immunized
 Destruction of stray dogs and cats
 Maintain active surveillance for rabies in domestic
animals

B. Specific prevention for human
Post-exposure prophylaxis
1- Management of wound
Treatment after exposure, known as post-exposure
prophylaxis (PEP), is highly successful in preventing the
disease if administered promptly, in general within ten days
of infection. Thoroughly washing the wound as soon as
possible with soap and water for approximately five
minutes is very effective in reducing the number of viral
particles. "If available, a virucidal antiseptic such as
povidone-iodine, iodine tincture, aqueous iodine solution,
or alcohol (ethanol) should be applied after washing.

2- Seroprophylaxis
Half at site of wound (infiltration)
And the rest IM GLUTEAL (away from site of animal
bite )
HRIG Human rabies immunoglobulin :20IU Per KG
ERIG Equine rabies immunoglobulin: 40 IU per KG
3- Observing the animal
4- Post exposure vaccination

Rabies vaccines
A. Human diploid cell vaccine (HDCV)
B. Rabies vaccine adsorbed (RVA)
C. Purified chick embryo cell vaccine(PCEC)
DOSE : 1ml IM in deltoid or upper outer thigh in
infants. 5 doses 0, 3 , 7 , 14 , 28-35 days if immunized
only 2 doses 0 , 3 days
Chemoprophylaxis : penicillin or antibiotic to prevent
wound sepsis.

Pre exposure prophylaxis
In high risk groups sach as veterinrians , animal
handlers , and certin laboratory workers
Dose : 0 , 7 , 21 days booster every 2 years

Control
Cases :
 Notification
 Isolation and hospitalization
 Treatment : supportive
 Concurrent disinfection of patient s discharge
Contacts:
 Enlistment
 Surveillance of contacts and animals
 Wearing PPE to prevent contact with patient saliva

DEFINITION
Acute disease from wound infection witch is caused
by
clostridium tetani exotoxins
OCCURRENCE
1 million annually , underdeveloped countries
Neonatal tetanus accounts 50 % of tetanus related
death

Pre pathogenic period
Agent : Clostridium tetani a mobile
Spore-forming anaerobic , gram positive
Bacillus,
Reservoir: Intestines of horses and other animals
and man.
Exit : intestinal excreta
Source of infection: soil , dust, clothing skin 10-15%
of human GIT

Mode of transmission:
 Neonatal tetanus
Cord contamination
 Cephalic tetanus
Head trauma , otitis media
 Local and generalized tetanus
Wound injury (contaminated with soil)

Entry : skin , wound , burn , or contaminated
injection.
Pathogenic period :
3 – 21 days ( 14 days )

Clinical picture: 4 clinical type
Neonatal tetanus (tetanus neonatorum):infected infants
become irritable, feed poorly, and developed rigidity
with spasms (very poor prognosis for survival)

Local tetanus: persistent muscle contractions in the
same anatomic area as the injury, which will however
subside after many weeks; very rarely fatal; milder
than generalized tetanus, although it could precede it.
Cephalic tetanus: occurs with ear infections or
following injuries of the head; facial muscles
contractions.

Most common types: Generalized tetanus
 -descending pattern: lockjaw  stiffness of neck
 difficulty swallowing  rigidity of abdominal
and back muscles.
 -Spasms continue for 3-4 weeks, and recovery can
last for months
 -Death occurs when spasms interfere with
respiration.

Tetanic seizures (painful, powerful bursts of muscle
contraction)
 if the muscle spasms affect the larynx or chest wall,
they may cause asphyxiation
 stiffness of jaw (also called lockjaw) RISUS
SARDONICUS
 stiffness of abdominal and back muscles
OPISTHOTONOUS
 contraction of facial muscles IRONIC SMILE
 fast pulse
 fever
 sweating

diagnosis
•Based on the patient’s account and physical
findings that are characteristic of the disease.
Diagnostic studies generally are of little value, as
cultures of the wound site are negative for C. tetani
two-thirds of the time.
–When the culture is positive, it confirms the
diagnosis of tetanus

Fatality
Neonatal tetanus : 90%
Mild and moderate : 6%
Sever tetanus: 60%
Prevention
General prevention
Health education ,personal hygiene, environmental
sanitation , complete of immunization dose
,socioeconomic development

Specific prevention
DPT : 2, 4, 6 ,18 months, DT at school age , and
booster shot every 10 years.
Immunization of pregnant female with tetanus
toxoid : 2 doses (2 doses1 month interval after first
trimester).
Delivery under complete aseptic condition

Control
Cases :
 Early case finding, Notification
 Hospitalization but not isolation
 Treatment :
 Remove and destroy the source of the toxin through surgical
exploration and cleaning of the wound (debridement).
 Passive immunization with human tetanus immune globuline
(TIG) 500 U
 Bed rest with a non stimulating environment (dim light,
reduced noise, and stable temperature) may be
recommended.

 Sedation may be necessary to keep the affected
person calm.
 Respiratory support with oxygen, endotracheal tube,
and mechanical ventilation may be necessary.
Contacts:
 Investigation of of contacts and source of infection
to determine the circumstances of injury

Agent
• Caused by B anthrax a gram-positive spore
forming rod, aerobic
• Spore if very hardy can survive for decades in
the soil killed by heat at 160 c for 1 hour

Source of infection
• Contracted by contact of abraded skin with products
of infected cattle, sheep and goats
• Products include hides ‫,الجلود‬ hair, wool‫الصوف‬ , bone
and meat.
Mode of transmission
Coetaneous anthrax :direct contact with the infected
animals
Gastrointestinal Anthrax is very rare and occurs from
consuming infected meat

Inhalational anthrax pneumonic(wool sorter’s
disease) :
from inhalation of spores from textile ‫والنسيج‬ ‫االغزل‬
and slaughterhouse workers ‫السلخانة‬
Incubation period : hours to 7 days

Clinical picture
Cutaneous anthrax
• Progression of painless lesions
Papule/macule – pruritic
Vesicle/bulla – clear or serosanguinous
Ulcer – non pitting, gelatinous edema
black, depressed, rarely scars,
24-48 hrs.
days

Intestinal anthrax
Affect cecum primary cause multiple ulcers
make patient complain of :
 Fever , nausea , vomiting.
 malaise , anorexia, abdominal pain
 hematemesis and bloody diarrhea.

Pneumonic anthrax
 Hemorrhagic mediastinitis
 Pulmonary edema
 Hemorrhagic plural effusions
 Increase among wool sorters( (‫الصوف‬ ‫فرز‬
Bloodstream invasion may cause septicemic
anthrax which may lead to death. Internal organs
become darkly colored with widespread
petechiae and hemorrhage

Diagnosis
Isolation of the causative bacilli in blood, lesion or
discharge and serologic test
Complication
 Persistent circular scar at the site of
lesion(cutaneos anthrax)
 Fatality rate 100% in pneumonic anthrax

Prevention
General prevention
Measure to prevent occupational infection:
(PPE, washing facilities, health education, vaccination)
Measure to animal :
Veterinary supervision, vaccination of animals , quarantine
measures in case of an animal outbreaks
Measure to animal products:
Only health animal are slaughtered
Hair and wool adequate disinfection, imported wool must
have a certificate of freedom anthrax

Specific prevention
1. Human
Vaccination : cell free vaccine for high risk persons
2. Animals
 vaccination
 diseased animals :isolation, disinfection of
discharge, treatment with penicillin

Control
Cases:
 Early case finding
 Notification ,isolation in hospital
 Concurrent , terminal disinfection(steam, corrosive,
burn)
 Treatment :penicillin drug of the choice, ciprofloxacin
for 10 days in (cutaneous anthrax ) and 60 days in bio-
terrorist attack (pneumonic anthrax)

Contacts
 Enlistment
 Surveillance for maximum incubation period
 Isolation of contacts of pneumonic anthrax for 7
days
Environment
 Concurrent , terminal disinfection
 Investigate the source of infection
 Outbreak control measures
 Combating bioterrorism

Contact zoonotic disease

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