DOG BITE and it's Management-RAVINDRA G O

SEMINAR
Presenter: Dr Ravindra G O
Moderator: Dr Jagadish S
1

TOPIC: DOG AND
OTHER ANIMAL BITES
2

OVERVIEW
• Introduction
• Epidemiology
• Mechanisms of injury and clinical features
• Approach to diagnosis
• Complications
• Treatment
3

Introduction
• Mammalian bites can cause either direct injury
due to bite or scratch or can lead to secondary
damage due to super added infections.
• Dog bites are the most common.
• Human and cat bites are more likely to get
secondary bacterial infection.
4

• In addition to the usual concern of Rabies some
exotic infections to be concerned about various
bites are as follows
a) Rat bite fever very rare illness 1 to 3 weeks
of incubation period. Associated with fever,
chills, and rash.
b) Cat scratch fever is rare occurs 3-10 days of
incubation period.
starts as crusted papule at site of scratch
Tender lymphadenopathy.
5

Can present as encephalopathy ,pneumonia, or
parotid swelling.
c) rabbit bite can cause tularemia.
All unprovoked mammalian bites are a concern for
rabies especially-dogs , monkeys, wild canines
and bats.
Rabbit and rodents bites do not need post
exposure rabies prophylaxis.
6

Scope of the problem
• No global estimate of dog bite incidence, but
studies suggest that dog bite accounts for ten
millions of injuries annually.
• In US, 4.5 million people are bitten by dog every
year.
Of these, nearly 885000 seek medical care;
30000 have reconstructive procedures
3-18% develop infections and between
10 to 20% fatalities occur.
7

Animal bites
• An estimated 17.4 million small animal
bites occur in INDIA every year
• In community based study In delhi ,overall
incidence of small animal bites was 8/1000
population/year.
• Incidence for minor and major injuries was
2.5/1000 and 5.3/1000, respectively
8

• In a multicentric study from Six cities of
INDIA over 18 months
Dog bites-MC(92%,mostly stray ones)
Monkey bites(3.2%)
Cat (1.8%)
Fox(0.8%) among 1357 fresh bite
injuries.
Half of them were children(2-8 yrs) and
mostly unprovoked(64.3%)
9

• Seasonal pattern of dog bite;
peak incidence-10 weeks following the
peak stray-dog breeding period, due to
maternal protective behaviour of stray dogs.
• Fatalities from dog bites are more in low-
and middle-income countries due to poor
primary health care infrastructure and lack
of access to post exposure management.
10

Who is most at risk?
• Children make up the largest percentage of
people bitten by dogs, with the highest incidence
in mid – to –late childhood.
• The risk of injury to the head and neck is greater
in children than in adults, adding to increased
severity, necessity for medical treatment and
death rates.
• In some countries ,males have higher frequency
of dog bites than females
11

Dog bite
• The microbiology of infected bite wounds from
dogs is similar to that of the organisms that
colonize the dog’s oral cavity.
• Less frequently, isolates may also come from the
environment and patients skin.
• Both clinically infected and early-presenting(less
than 8hrs post injury and/or not yet clinically
infected) dog bite wounds are poly-microbial, with
a broad combination of aerobic and anaerobic
microorganism.
12

Aerobic organisms;
• Pasteurella,
• Streptococcus
• Staphylococcus
• Neisseriae
• Corynebacterium
• Moraxella
• Enterococcus
• Bacillus.
Anaerobic organisms
• Fusobacterium
• Prevotella
• Propionibacterium
• Bacteroides
• Peptostreptococcus
13

• A majority of the infections were purulent
wounds without abscess formation (58%),
followed by nonpurulent wounds with
cellulitis, lymphangitis, or both (30%) and
abscesses (12%).
14

Background :RABIES
• Rabies is acute viral encephalitis transmitted by
exposure to rabid animals.
• Zoonotic disease
• One of the most dreaded disease
• When infection sets in, rabies is invariably fatal.
• On the other hand rabies is a vaccine
preventable disease, especially when vaccination
is combined with immunoglobulins.
15

Epidemiology
• Rabies is endemic in many Asian and African
countries.
• India is a high endemic country for rabies
• Only the island of andaman and nicobar in east
and lakshadeep islands in west are rabies free.
• Acccording to WHO estimates, about 50000
human deaths due to rabies are reported every
year in the world.
• About 20000 human rabies deaths occur in India
every year.
16

• Animal mainly responsible for human rabies is
dog.
• Reservoir of rabies virus
1. Dogs -96.3%
majority are stray dogs-76%
Pets-11.1%
2. Wild-3.5%
3. Otherwise or unknown -10.2%
17

Virus
• Bullet shaped , single
stranded enveloped RNA
virus.
• Family-Rhabdoviridae,
Genus-Lyssa virus.
• 12 genotypes classic
rabies virus(genotype
1),which has worldwide
distribution.
• Measures 100-300nm in
length depending on the
strain and 75 nm in
breadth.
• Is highly neurotropic virus.
18

• The rabies virus is resistant to
Cold temperature
Dryness And decays,
• But is rapidly inactivated by the action of
Oxidizing agents, Solvents,
Quaternary ammonium compounds,
Soap and Detergents as presence of lipid in
outer coat of rabies virus particle makes it
relatively easy to disrupt them by simply addition of
lipid solvent.
19

Reservoir;Cycles of rabies
• Foxes, raccoons,
skunks, jackals,
mongooses, bats,
etc
Sylvatic
cycle
• Dogs, cats, cattle,
horses, sheep, pigs
etc
Urban
cycle
20

Modes of Transmission of rabies Infection
1. Bites
2. Scratch
3. Lick on damaged skin and intact mucous
membrane by rabid animals
4. Organ transplant-cornea transplant mainly
5. Aerosol spread in bat infested caves.
21

Clinical Features
• Average incubation period varies between 3
weeks and 3 months.
• Its highly variable, may be short as 4 days to long
as 3 years.
• The size of the inoculum of virus and the bites in
head and neck region due to proximity to brain,in
hands due to excess innervations may have
some significance in early causation of the
disease.
23

Clinical forms
• Symptoms of spasm of
gullet-
hydrophobia,aerophasia and
aggressivenesscoma and
death in 3-5 days
Furious
type(80%)
• Progressive onset of
ascending paralysis.
• Order of involvementlower
limbs-abdominal muscles-
upper limb-thoracic muscles
f/b coma, RF and death.
Dumb or
paralytic
type(20%)
24

Classification of the bites
25

Management :Approach to Post-Exposure
Prophylaxis
Is a three pronged approach.
All three carry equal importance and should be
done simultaneously as per the category of
exposure.
1. Management of animal bite wound(s)
2. Passive immunization with Rabies
Immunoglobulin (RIG)
3. Active immunization with Anti-Rabies Vaccines
(ARV)
27

• Application of antiseptics:
After thorough washing and drying the wound(s),
any one of the available chemical viricidal agents
should be applied, such as povidone iodine,
alcohol, etc.
• Local inﬁltration of rabies immunoglobulin:
In category III exposures rabies immunoglobulin
should be inﬁltrated in the depth and around the
wound(s) to neutralize the locally present virus.
29

• Suturing of wound(s) should be avoided as far as
possible.
• If surgically unavoidable, after adequate
cleansing, rabies immunoglobulin should be
inﬁltrated in the depth and around the wound(s)
and suturing should be delayed by a few hours.
• The delay in suturing allows diffusion of
antibodies in the tissues.
• Minimum loose sutures should be applied for
arresting the bleeding in life threatening
situations.
30

• Cauterization of wound(s) is no longer
recommended as it leaves bad scar, and does not
confer any additional advantage over washing the
wound(s) with water and soap.
• Tetanus and antibiotic prophylaxis should be
given if required.
• To prevent sepsis in the wound(s), a suitable
course of an antibiotic may be recommended.
31

Rabies Immunoglobulin (RIG)
• The anti-rabies serum/Rabies Immunoglobulin
(RIG) provides passive immunity in the form of
ready-made anti-rabies antibodies, before it is
physiologically possible for the victim to begin
producing his/her own antibodies following anti-
rabies vaccination.
• Neutralization of virus present at the site of bite.
32

Rabies Immunoglobulin (RIG)
Equine Rabies
Immunoglobulin (ERIG):
• heterologous origin
produced by hyper-
immunisation of horses.
• Currently manufactured
ERIGs are highly puriﬁed
Fab 2' fragments and the
occurrence of adverse
events has been
signiﬁcantly reduced.
• Dose:40 IU/kg
• The ERIG produced in India
contains 300 IU per ml.
Human Rabies
Immunoglobulin (HRIG)
• homologous origin and are
relatively free from the side
effects.
• Because of their longer half-
life, they are given at half
the dose of equine anti-
rabies serum.
• Dose:20 IU/kg
• HRIG preparation is
available in concentration of
150 IU per ml.
33

Administration of rabies
immunoglobulin:
• The RIG should be brought to room temperature
(25ºC to 30ºC) before administration to the
patient.
• As much of the calculated dose of RIG as is
anatomically feasible should be inﬁltrated into
and around the wound/s.
• Multiple needle injections into the wound(s)
should be avoided.
34

• After all the wound(s) has been infiltrated, if any
volume of RIG is remaining, it should be
administered by deep intramuscular injection at a
site distant from the vaccine injection site.
• Dilution of RIG with normal saline to a volume
sufficient to infiltrate all the wounds in case of
Animal bite wounds in icted can be severe and
multiple, especially in small children.
35

• The total recommended dose of RIG must not be
exceeded as it may suppress the antibody
production stimulated by the anti-rabies vaccine.
• RIG should be administered only once, preferably
at, or as soon as possible after, the initiation of
PEP.
36
•Did you know:
• Even if RIG is not available at the first visit (PEP day
0),RIG can be given up to day 7 after the first rabies
vaccine administration.

• Rabies Immunoglobulin should never be
administered in the same syringe or at the same
anatomical site as vaccine.
• Animal bite victim should be kept under
observation for at least half–an–hour after
administration of ERIG. There is no need to admit
the patient.
• No need of skin test before administering ERIG.
37

Tolerance and side effects:
• There may be transient tenderness at the
injection site and a brief rise in body temperature
that does not require any treatment.
• Anaphylactic reactions are extremely rare. RIG
must never be given intravenously.
• Serum sickness is rare side effect.
38

Treatment of anaphylactic reaction
• Physicians administering ERIG should always be
ready to treat anaphylactic reactions with
adrenalin.
• The dose is 0.5 ml of 0.1 percent solution (1 in
1000, 1mg/ml) for adults and 0.01ml/kg body
weight for children, injected subcutaneously or
IM.
• Other emergency drugs and supportive therapy
should also be available.
39

Available RIG in India
1. FAVIRAB Injection
1. Cost -Rs.1780
2. Unit- 400 IU/ml
3. Quantity -5ml
2. IMORAB Injection
1. Cost-Rs.625
2. Unit 10000 IU/5ml
3. PARS injection
1. Cost- Rs. 625
2. Unit-10000 IU/ml
3. Quantity -5ml
42

Anti-Rabies Vaccines
• Vaccines are the mainstay for prevention of
development of the rabies.
• Since 1984, WHO has strongly recommended
discontinuation of production and use of nerve
tissue vaccines due poor efficacy and life
threatening adverse effects of neuro-paralytic
reactions.
43

Currently available vaccines
• The Cell Culture Vaccines(CCV) and include
Purified Chick Embryo Cell Vaccine(PCECV),
Human Diploid cell Vaccine(HDCV),
Purified Vero Cell Vaccine(PVRV)
• Purified Duck Embryo Vaccine(PDEV).
• It is absolutely essential that every batch of CCVs
have minimum potency of 2.5IU per IM dose,
irrespective of whether the vaccine is administered by
IM or ID route.
44

EFFICACY AND EFFECTIVENESS
• The vaccines are available in lyophilized form
with sterile water as diluent, are stable for 3 years
at 2 to 8°C and should be used within 6 hours of
reconstitution.
• All CCVs have almost equal efficacy and any one
of these can be used
• These vaccines induce protective antibodies in
more than 99% of vaccinees following pre-/ post-
exposure prophylaxis.
45

DURATION OF IMMUNITY
• The current CCVs possess immunological
memory after vaccination, and individuals who
had received their primary series 5–21 years
previously showed good anamnestic responses
after booster vaccination even when antibodies
are no longer detectable.
46

Adverse effects
• Local pain,
• Swelling
• Redness
• and less commonly fever, headache, dizziness
and gastrointestinal side effects.
• Systemic hypersensitivity reactions in vaccines
have been reported with HDCV particularly
following booster injections but not with PCEC/
PVRV.
• Intradermal vaccination may cause more local
irritation as compared to the (2)intramuscular
47

Switch over from one brand/type of vaccine to
the other:
• Shifting from one brand/type of CCV to other
brand/type should not be encouraged in routine
practice.
• However, under unavoidable circumstances,
available brand/type may be used to complete
PEP.
48

Anti-Rabies Vaccines
49
Indications:
• All animal bite victims of Category II and III
exposures irrespective of age and body weight
require the same number of injections and dose
per injection.
• All Category III exposures and Category II
exposures in immuno-compromised individuals,
in addition, require administration of RIG

WHO Position: Recommended Schedules
50

• one-week, 2-site ID regimen / Institute Pasteur du
Cambodge (IPC) regimen/2-2-2-0-0;
Duration of entire PEP course: 7 days.
• two week ,IM PEP regimen/4-dose Essen
regimen/1-1-1-1-0;
Duration of entire PEP course: between 14 to 28
days.
• three week,PEP regimen/Zagreb regimen/2-0-1-
0-1; Duration of entire PEP course: 21 days.
51

Pre-exposure prophylaxis
• WHO recommends PrEP for individuals at high
risk of RABV exposure:
– These include sub-populations in highly
endemic settings with limited access to timely and
adequate PEP.
– Individuals at occupational risk
– Travellers who may be at risk of exposure
57

• PrEP should be considered in sub-populations
living in remote, rabies endemic areas, where the
dog bite incidence is >5% per year or vampire bat
rabies is known to be present.
• WHO recommends the following PrEP schedule:
– 2-site ID vaccine administered on days 0 and
7.
– 1-site IM vaccine administration on days 0 and
7
58

• For both PEP and PrEP, vaccines can be
administered by either the ID or IM route.
– One ID dose is 0.1 mL of vaccine;
– One IM dose is 0.5 mL or 1.0 mL depending.
on the product, i.e. the entire content of the vial.

.Frequently Asked Questions
Q1.Application of chillies, lime, salt and mustard oil to
animal bite wound is common practice. Does it confer any
advantage over washing with soap and water?
Q2. Are there any dietary restrictions for animal bite victims
receiving anti-rabies vaccination?
Q3. Can a vaccinated dog transmit rabies?
Q4.It is necessary to perform an antibody test following
antirabies vaccination in all animal bite victims?
60

Monkey bites
• Second most common small animal bite in
SA, and pose important risk to travellers
and tourists.
• Assumes significance as monkeys are
supposed to be regular carriers of rabies
virus.
61

ETIOLOGY:
AGENT:-
Monkeypox virus, causing the disease
monkeypox, is the most important member for
humans of the genus Orthopoxvirus since the
eradication of smallpox (variola).
62

• Monkeys are the predominant host for the virus.
• It may be endemic in African rainforest squirrels
and is present in African rats, mice, domestic
pigs, hedgehogs, and opossums.
• It also has been identified in and transmitted by
prairie dogs in the United States, and has
affected elephants in zoos.
63

64
A, Legs and feet of monkeypox patient. B, Legs and feet of smallpox
patient at similar stage of rash (pustular)

Clinical course
• The clinical signs, symptoms, and course of
monkeypox are similar to those of smallpox,
although typically milder.
• After a 10-14 day incubation period during which
the virus replicates in lymphoid tissues,
• Humans experience an abrupt onset of malaise,
fever, myalgia, headache, and severe backache.
.
65

• Nonproductive cough, nausea, vomiting, and
abdominal pain may be present.
• Generalized lymphadenopathy, a finding unusual
in smallpox, is invariably present during the acute
stages of monkeypox illness
66

• After a 2-4 day prodrome, an exanthem appears
in cephalad-to-caudal progression.
• As the rash progresses, fevers begin to abate.
The rash is initially macular, but transforms within
hours to firm papules that rapidly vesiculate and
become pustular over 2-3 days.
• Unlike smallpox lesions, but similar to chickenpox
lesions, the lesions of monkeypox tend to occur in
crops.
• Late into the 2nd wks of illness, the lesions begin
to desiccate, crust, scab, and fall off.
67

Diagnosis
• Isolation of monkeypox virus in culture,
• Demonstration by polymerase chain reaction of
viral DNA in a clinical specimen,
• Microscopic demonstration of an orthopoxvirus in
a clinical specimen in the absence of other
orthopoxvirus exposure.
68

Treatment
• There is no proven effective therapy for
monkeypox.
• Despite evidence that pre-exposure
administration of smallpox vaccine is 85%
effective in preventing or attenuating monkeypox
disease, the rarity of monkeypox infection does
not warrant universal vaccination.
• For prevention of human-to-human spread of
disease, a combination of contact, droplet, and
airborne infection control procedures should be
69

Cat bites
• Also contribute a significant number in
Indian studies on small animal bites.
• These tends to be provoked, with female
being more likely victims.
70

Cat Scratch Disease(CSD)
• Affect both normal and immunocompromised
hosts.
• 80 % of cases occur in children.
• Linked to exposure to cats, especially kitten and
cats with fleas. CSD can result from a cat scratch
or bite, as well as from a fleabite.
71

• Characterized by self-limited regional
lymphadenopathy near the site of organism
inoculation.
• Occasionally life threatening manifestations (5-
14%) include visceral organ, neurologic, and
ocular involvement because of the dissemination
of organism.
• In AIDS patients: Bacillary angiomatosis.
72

Diagnosis :
• a positive B. henselae antibody titer or
• a positive Warthin Starry stain or
• PCR analysis of tissue.
• Very difficult to isolate from tissue specimens
74

Treatment
• Antibiotics are not indicated in most cases but they
may be considered for severe or systemic disease.
• Reduction of lymph node size (no REDUCTION in
the duration of symptoms) has been demonstrated
with a 5-day course of azithromycin and may be
considered in patients with severe, painful
lymphadenopathy.
• Immunocompromised patients should be treated with
antibiotics:
• Trimethoprim-sulfamethoxazole,Gentamicin,
Ciprofloxacin,Rifampin
• B. henselae is generally resistant to penicillin &
75

RAT BITE FEVER
• Rat bite fever caused by Streptobacillus
moniliformis is most commonly reported in the
United States, as well as in Brazil, Canada,
Mexico, Paraguay, Great Britain, and France; it
has been identified elsewhere in Europe and in
Australia.
• S. moniliformis is a Gram-negative bacillus that
is present in the nasopharyngeal flora of many
laboratory and wild rats.
76

• Rat bite fever caused by Spirillum. minus,
called sodoku, is most commonly reported in
Asia.
• S. minus is a small, spiral, aerobic Gram negative
organism.
• Reports of rat bite fever from Africa are rare,
suggesting under recognition rather than absence
of the disease.
77

Transmission of infection
• Infection with S. moniliformis most commonly
occurs following the bite of a rat;
• Also when scratched by rats, in those who have
handled dead rats,
• Ingested milk contaminated with the bacterium
(termed Haverhill fever).
• Rat bite fever may also be transmitted by bites
from wild mice.
78

• Incubation period is variable, ranging from 3-10
days.
• The illness is characterized by an abrupt onset of
fever up to 41°C (105.8°F) (fever occurring in
more than 90% of reported cases),
severe throbbing headache,
intense myalgia,
chills, and vomiting
• The lesion at the cutaneous inoculation site has
healed by the time the systemic systems first
appear.
79

Rash(75%)
• The rash consists of blotchy, red maculopapular
lesions that often have a petechial component.
• The distribution of the rash is variable but is
typically most dense on the extremities.
• Hemorrhagic vesicles may develop on the hands
and feet and are very tender to palpation.
80

Polyarthritis
• Approximately 50% of patients have arthritis,
which first manifests toward the end of the 1st wk
of disease; early on, the arthritis may be
migratory.
• If untreated, fever, rash, and arthritis last from
14-21 days, often with a biphasic pattern to the
fever and arthritis.
82

Diagnosis –
• Gram or Giemsa stain blood, joint fluid, pus.
• – Culture
• – Serology
• – PCR
83

Complications
• Pneumonia,
• Persistent arthritis,
• Brain and soft tissue abscesses, and,
• less commonly, myocarditis or endocarditis.
• The mortality rate of untreated rat bite fever is
estimated to be approximately 13%.
84

Treatment
Penicillin is the drug of choice for both forms of rat
bite fever.
• Intravenous penicillin G or intramuscular penicillin
G procaine is recommended for 7-10 days;
• a regimen of IV penicillin G for 5-7 days followed
by oral penicillin V for an additional 7 days has
also been used.
• Doxycycline, gentamicin, or streptomycin
represent effective alternatives for penicillin-
allergic patients.
85

• Patients with endocarditis caused by S.
moniliformis require high-dose penicillin G for 4
wk; the addition of streptomycin or gentamicin
might be helpful.
86

others
• Mongoose in rural areas
• Camel in rajasthan and haryana
• Black bear in himalayan territories
• Large cats(tiger,lions,leopards) in wild and in
various bioreserves
• Wild dogs,hyenas,wolves, crocodiles, and other
reptiles.
87

Human bite
HIV, HBV infection following human bite
• Any unvaccinated patient or individual negative
for anti-HBs antibodies who is bitten by an
individual positive for HBsAg should receive both
hepatitis B immune globulin (HBIG) and hepatitis
B vaccine.
88

• If the source is unknown or not available for
testing, the clinician should initiate the hepatitis B
vaccine series.
• In addition, although the risk for transmitting HIV
through saliva is extremely low, infection is of
concern if there is blood in the saliva. Counseling
regarding post-exposure HIV prophylaxis is
appropriate in this setting.
89

Eikenella corrodens
• Anaerobic small GN bacilli
• Common in human oral flora
• Resist to: – Cephalexin, Clindamycin,
Erythromycin, Metronidazole.
• Susceptible to: – Amoxy-clav, FlouroQuinolones,
TMP/SMX, Doxycycline.
90

Tularemia
• F. tularensis can survive in water, soil, and
decaying animal carcasses for a long time.
6 Presentations
• Typhoidal
• Pneumonic
• Oculoglandular
• Oropharyngeal
• Ulceroglandular
• Glandular
91

• Treatment: –
Streptomycin 30 mg/kg qd IM for 10‐14 days,
or
Gentamicin 3‐5 mg/kg qd IV for 10‐14 days.
92

Summary
• Wash the wound thoroughly with soap and water
for 10- 15 minutes.
• Do not bandage.
• Do not suture.
• Tetanus vaccination
• Rabies vaccination only for 2nd degree and RIG and
vaccination for 3rd degree wounds.
• Amoxy-clav. for 3rd degree wounds.
• Wound care is most important
• If unavoidable, you can suture
• No time period for vaccination
94

Reference
• National Rabies Control Programme /National Guidelines
on Rabies Prophylaxis ( by NATIONAL CENTRE FOR
DISEASE CONTROL).
• www.who.int/immunization/documents/positionpapers/rabi
esvaccine/feb2018
• Kliegman/Stanton/st Geme/Schor/Nelsn text book of
pediatrics/edition20/volume2/pg no 3447to3457.
• Piyush gupta/2nd edition/volume1/pg no 389-391
• Karin Rothe, Michael Tsokos, and Werner
Handrick/Animal and Human Bite Wounds /Deutsches
Ärzteblatt International | Dtsch Arztebl Int 2015; 112: 433–
43
95

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