DOG BITE and it's Management-RAVINDRA G O

Seminar prepared under the guidance of Dr Jagadish S . Based on latest WHO guidelines

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

2. Topic: Dog and other Animal bites 2

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

4. 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

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

6. C an 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

7. 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 oc cur . 7

8. 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

9. 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

10. 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

11. 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

12. 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

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

14. 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

15. 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

16. 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

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

18. 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

19. 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

20. Reservoir;Cycles of rabies 20

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

22. Pathogenesis 22

23. 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

24. Clinical forms 24

25. Classification of the bites 25

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27. 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. Management of animal bite wound(s) Passive immunization with Rabies Immunoglobulin (RIG) Active immunization with Anti-Rabies Vaccines ( ARV) 27

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29. 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

30. 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

31. 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

32. 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

33. 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

34. 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

35. 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

36. 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.

37. 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

38. 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

39. 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

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

43. 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

44. 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

45. 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

46. 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

47. Adverse effects L ocal pain, S welling R edness 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 route. 47

48. 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

49. 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

50. WHO Position: Recommended Schedules 50

51. 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

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55. Post –Exposure prophylaxis

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57. 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

58. Pre-exposure prophylaxis 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

59. Pre-exposure prophylaxis 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.

60. .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

61. 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

62. 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

63. Monkeys are the predominant host for the virus. I t 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. 64 A, Legs and feet of monkeypox patient. B , Legs and feet of smallpox patient at similar stage of rash ( pustular )

65. 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, H umans experience an abrupt onset of malaise, fever, myalgia, headache, and severe backache. . 65

66. 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

67. 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

68. Diagnosis I solation of monkeypox virus in culture, D emonstration by polymerase chain reaction of viral DNA in a clinical specimen, M icroscopic demonstration of an orthopoxvirus in a clinical specimen in the absence of other orthopoxvirus exposure. 68

69. 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 implemented. 69

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

71. 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

72. 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

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74. 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

75. 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 & amoxicillin 75

76. 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

77. 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

78. 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 , I ngested milk contaminated with the bacterium (termed Haverhill fever ). Rat bite fever may also be transmitted by bites from wild mice. 78

79. 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 T he lesion at the cutaneous inoculation site has healed by the time the systemic systems first appear. 79

80. Rash(75%) T he rash consists of blotchy, red maculopapular lesions that often have a petechial component. T he 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

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82. 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

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

84. Complications Pneumonia , P ersistent arthritis, B rain 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

85. 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

86. 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

87. 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

88. 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

89. 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

90. 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

91. 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

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

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94. 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

95. Reference National Rabies Control Programme /National Guidelines on Rabies Prophylaxis ( by NATIONAL CENTRE FOR DISEASE CONTROL). www.who.int/immunization/documents/positionpapers/rabiesvaccine/feb2018 Kliegman / S tanton/ st Geme / Schor / Nelsn text book of pediatrics /edition20/volume2/ pg no 3447to3457. Piyush gupta /2 nd 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