電子期刊

ISSN:1684-193X

Abstract

Introduction

1. Open wounds should be irrigated with copious volumes of normal saline as soon as possible. The preferred way is to use high pressure irrigation with normal saline or lactated ringers via a 19 gauge needle and large syringe.
2. The police should be notified of the incident.
3. When possible, tetanus toxoid and rabies vaccination status should be determined for all animal bites. (The rabies vaccination is not recommended in Taiwan)
4. Assess the extent of damage to the tissues including joint involvement, consider a roentgenogram to rule out a fracture if suspected, determine the need for cosmetic repair, stratify the patient for risk factors of infection, obtain wound cultures if infection is suspected (i.e. fever, erythema at injury sites, and observe necrosis or purulent wound drainage).¹¹ (Table 3)

Infections caused by animal bites are often polymicrobial, with an average of three to five bacterial species isolated per wound culture.
Staphylococcus spp., Streptococcus spp., Corynebacterium and various gram-negative enteric pathogens are the most commonly identified aerobes. Bacteroides spp., Fusobacterium, Peptostreptococcus, Actinomyces, Veillonella parvula and Eubacterium are commonly identified anaerobic organisms (11)

It has been suggested that antibiotic serum concentrations should be therapeutic within 3 hours after the injury. The recommended duration of prophylactic therapy with oral agents is a period of 5-7 days.
Those with more severe wounds, diabetes, vascular disorders, or who are immunocompromised may require a more aggressive approach with oral or parenteral antibiotics. The selection of an antibiotic regimen should follow the same criteria of empiric therapy of an infected bite wound.

An appropriate empiric antibiotic regimen must direct at the pathogens most likely to cause infection, including both aerobic and anaerobic bacteria. Therapy should target organisms from both the oral cavity of the animal, as well as potential pathogens from the skin flora of the victim.
Indications for hospital admission include signs of sepsis, fever, significant edema or crush injuries, spreading cellulitis, involvement of a bone, joint, tendon or nerve, failed outpatient therapy, and immunocompromised hosts. Intravenous therapy may also be necessary in patients with known histories of medication non-compliance.
The most common agent for mammalian bites is monotherapy with amoxicillin/clavulanate owing to the additional anaerobic coverage offered by the [beta]-lactamase inhibitor. Alternative regimens include clindamycin plus ciprofloxacin, dicloxacillin plus penicillin, tetracyclines, trimethoprim/sulfamethoxazole, and second- or third-generation cephalosporins such as cefuroxime.¹¹ (Table 4)

Rabies cannot be treated. Therefore, efforts must focuse on prevention.
1. Rabies immunization for domestic animals
2. Education about avoiding contact with wild animals is an important public health issue on reducing risk of rabies exposure. Raccoons, skunks, foxes, and coyotes can be enjoyed from a distance, but they should not be attracted intentionally or adopted.

Passive Vaccination---RIG is a solution of globulins dried from the plasma or serum of selected adult human donors who have been immunized with rabies vaccine and have developed high titers of rabies antibody.
RIG is administered to previously unimmunized people so that passive antibodies are present until the person begins making active antibodies to the vaccine. RIG should not be given more than 7 days after initiation of the vaccine because RIG may decrease a person's own antibody response. RIG is given in a single dose of 20 IU/kg body weight. After the initial vaccine is given, the 4 subsequent doses should be given on days 3, 7, 14, and 28. The production of specific antibodies against rabies virus requires about 7 to 10 days to develop.
Active Vaccination---Three rabies vaccines are currently available in the United States: rabies vaccine adsorbed, human diploid cell rabies vaccine, and purified chick embryo cell vaccine; all 3 are inactivated virus vaccines.
Patients who are taking corticosteroids or are immunosuppressed may not develop active immunity with the vaccine. Antibody titers may need to be monitored.
No evidence has shown that RIG or the rabies vaccine causes fetal abnormalities. Therefore, pregnancy is not a contraindication to appropriate rabies prophylaxis. RIG and the rabies vaccine have been used without problems in infants.^{13, 14, 15}(Table 5)

The tetanus bacillus is a Gram-positive, anaerobic rod that may develop a terminal spore, giving it a drumstick appearance. They can survive in soil for years and may be found in house dust, soil, salt, fresh water, and the feces of many animal species.
After into tissues, spores convert to vegetative forms, multiply, and elaborate tetanospasmin. Tetanospasmin enters the peripheral nerve at the site of entry and travels to the central nervous system (CNS) through the nerves or is transferred by the lymphocytes to the CNS. The toxin binds to gangliosides at the presynaptic nerve ending in the neuronal membrane, prevents release of neurotransmitters, and affects polarization of postsynaptic membranes in complex polysynaptic reflexes. The lack of inhibitory impulses that results is manifested in the characteristic spasms, seizures, and sympathetic overactivity of tetanus. The toxin has no effect on the mental status, so consciousness is not impaired directly by this illness.
The length and the course of the illness are determined by the location and amount of the bound toxin. The complete course of tetanus takes usually from 2 to 4 weeks and is in fluenced by patient age and the development of complications.

It is the most common form of clinical tetanus. It may occur after relatively minor injuries and often follows tetanus-prone wounds. The typical initial findings of trismus due to spasm of the parapharyngeal and masseter muscles are seen in 50% of cases.
Common complaints are pain, swallowing difficulty, and unilateral or bilateral stiffness of the neck and other muscle groups, such as those of the abdomen or thorax.¹⁷ Persistent trismus accounts for the risus sardonicus that is considered a classic finding of tetanus. As the illness progress, additional muscle groups become involved. One of the most striking findings occurs with spasm of the paraspinal musculature, which may result in severe opisthotonos. All voluntary muscles can be affected and the disease may involve the larynx, which can be fatal. Minor stimuli including light, drafts, noises or voices, and light touch may trigger spasms.
The effect of tetanospasmin on the autonomic nervous system can induce cardiovascular instability. Labile hypertension and episodes of tachycardia or other tachyarrhythmias are common. The sympathetic overactivity or superinfections, such as pneumonia can cause fever. Spasms and cardiovascular complications occur most commonly during the first week and resolve slowly during the ensuing 2 to 4 weeks.

The classic presenting complaints in tetanus consist of muscle spasms, trismus, stiffness, pain with dysphagia and cranial nerve weakness. These can be seen in other conditions.
The lack of altered consciousness in tetanus is an important point of differentiation from CNS infections, and a parapharyngeal inflammation can be diagnosed by clinical examination and/or radiographs of the airway.
Specific diagnosis of tetanus by routine laboratory tests is difficult. Gram stains and anaerobic cultures of wounds reveal the characteristic Gram-positive bacilli with terminal spores in as many as one third of tetanus patients. Although a positive wound culture can support the clinical diagnosis, a positive culture in the absence of symptoms does not indicate that tetanus intoxication will develop.

The worldwide mortality rate for generalized tetanus ranges from 45% to 55%. Although survivors generally do not experience neurologic sequelae, prolong convalescence with residual muscle rigidity is seen for several months.
The main predictors of prognosis are the rapidity of symptom onset and the rate of progression from trismus to severe spasms. Poor outcome is predicted by an interval between injury and trismus shorter than 7 days.

In Asia the causative organism is usually Spirillum minus, a small, spiral gram-negative organism. Children account for more than 50% of rat bite fever cases. In the United States rat bite fever is caused primarily by transmission of Streptobacillus moniliformis, a pleomorphic gram-negative rod .
Rat bite fever can be divided into 3 clinical syndromes. 1. Rat bite fever caused by Streptobacillus moniliformis infection, which is the predominant form seen in the United States. 2. “Soduku” caused by Spirillum minus, seen primarily in Asia. 3. When the clinical syndrome follows S moniliformis ingestion via contaminated food it is called “Haverhill fever. “