Cutaneous anthrax: An Indian perspective

Devinder Mohan Thappa, Kaliaperumal Karthikeyan

 Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry - 605 006, India

Correspondence Address:
Devinder Mohan Thappa
Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry - 605 006
India

Introduction

Anthrax, a toxigenic zoonosis of herbivorous animals in which humans are an incidental host, usually manifests in cutaneous form in man.[1] Though, the disease has become rare, endemic outbreaks occur in tropical countries, parts of South America, Europe where veterinary control of livestock is marginal and environmental conditions favour an animal-soil-animal cycle.[1],[2]

Many species of animals can be infected with Bacillus anthracis either natural or experimentally.[3] There is little doubt that the most important source of the infection is domestic herbivores. These species-cattle, sheep, horses, and goats- appear to be most susceptible to natural infection, whereas pigs and dogs, like humans, can be infected only when exposed to relatively large numbers of spores. Infection in most domestic species arises chiefty by ingestion of spores. A characteristic of anthrax in animals is the inability of blood to clot, as demonstrated by blood draining from the natural orifices of dead animals and skinned carcasses; this further increases soil contamination, the source of infection for animals. [3],[4]

Sources of infection

Human disease is most likely to occur in endemic regions by direct contact with infected carcasses.[5],[6],[7] Industrial cases may occur anywhere and reflect exposure to imported animal carcass products, such as bone meal (Which is used for making glues or fertilizer), hair, or hedes. Humans acquire infection by direct inoculation of spores through breaks in the skin, by inhalation of spores (generated during the early stage of cleaning contaminated goat hair), or by ingestion of contaminated meat. There may be some person-to person spread in peculiar circumstances. Direct abdomen to abdomen contact was resposible for the acquisition of infection in one of our child, the other child might have aquired the infection as a result of insect. [8] An outbreak in the Gambia was in part traced to the use of communal loofahs when bathing, and in the UK and Russia shaving brushes have been a source. [5] During the recent outbreak of anthrax in Zimbabwe and India, there were numerous anecdotal reports of human cutaneous anthrax associated with "fly bites".[9],[10],[11],[12],[13],[14],[15],[16],[17],[18]

Epidemiology of human anthrax in In-dia

In the developed nations, anthrax has all but disappeared. However, in India, which has got the largest population of livestock in the world, the disease is still endemic. [19] Seventy percent of its population is living in the villages, majority are dependent on livestock for their livelihood. Moreover, a large number of people working in the tanneries and leather industries have a chance of getting infected. [20]

The incidence of anthrax in animals and in man throughout India is not known accurately due to the fact that a large number of cases go unreported and only a fraction of human cases receive medical attention in a hospital. [20] Cases treated " on site" in a village are hardly ever brought to the notice of the authorities. Hence, the true incidence of anthrax in man is likely to be higher than reported in the literature. Detailed information collected from three Southern Indian states, Andhra Pradesh, Karnataka and Tamil Nadu have confirmed the endemicity of anthrax.

During the last two decades, about 70 cases of human anthrax have been encountered at Christian Medical College, Vellore, of which 26 cases had cutaneous anthrax. [21] A review of Indian literature in 1996, has found 112 cases of anthrax (71 cutaneous anthrax cases) in places other than Vellore. [20] We have recorded a series of 17 cases of cutaneous anthrax between July 1998 to September 2000 at JIPMER hospital, Pondicherry[8],[15],[16],[17] and an additional 6 cases till July 2001. [18] Date obtained from Animal Husbandry Department and Rajiv Gandhi College of Veterinary Sciences at Pondicherry revealed endemic outbreaks of anthrax amongst cattle′s, goats, sheep etc in Pondicherry and adjoining, Villupuram district of Tamil Nadu state for last 2 years (personal communication). Infected dying animals had bleeding from various orifices and characteristic splenomegaly.

Microbiology of B. anthracis

B. anthracis is a large, non-motile, brick-shaped, Gram-positive organism (2. 5x10mm), which occurs singly or in pairs in tissue. [1],[20] The so-called classical "boxcal" apperance of long strings of bacilli is seen only in culture. On methylene blue staining, the bacterial cell is stained blue, whereas the surrounding capsule is pink. This is described as the M′ Fadyean reaction. B. anthracis has the capacity to produce heat-and dry-resistant spores under adverse conditions.

The organism grows well on blood agar plates. Individual colonies are stickly and stand up in stalegmite-like forms when they are lifted or touched with a bacteriologic loop. [2] All the virulent strains of the bacillus are pathogenic for mice.

Pathogenesis

Locally, at the site of inoculation in the skin, pharynx, or intestine, low-level germination, growth, and production of exotoxins by the organisms result in extensive tissue edema and tissue necrosis due to vascular thrombosis. [22] In cutaneous anthrax, occasionally massive edema may result in hemoconcentration and hypotension. [23] In a small number of cases, systemic anthrax can lead to meningeal involvement by means of lymphatic or hematogenous spread. [4]

Clinical features

Anthrax occurs in three clinical forms in humans: 1) cutaneous anthrax due to direct contact with contaminated meat, carcasses, hides, hair, wool or bone, 2) inhalational anthrax (Woolsorter′s disease)due to inhalation of spores and 3) gastrointestinal anthrax due to ingestion of contaminated meat or milk. Anthrax meningitis occurs secondary to skin lesions, but it can complicate the other two forms also. [1],[4] Cutaneous anthrax accounts for 95% of all anthrax infections. More than 90% of lesions occur in exposed areas, such as the face, neck, arms, or hands. [4],[22] In children, cutaneous anthrax is more common on the head and neck. [1],[17] This may be due to deposition of spores and bacilli on abrasions by houselifes and vectorborne transmission by blood sucking insects (mosquitoes and stable flies). [1],[3]

Cutaneous anthrax usually begins as a painless, pruritic paplue within 3 to 10 days of inoculation. It rapidly progresses into a serous serosanguineous vesicles, which ulcerate with a central black eschar (Greek anthrakos-col), surrounded by a ring of vesicles within 36 hours [Figure - 1]. Perilesional oedema can be extensive [Figure - 2]. Toxic features occur in 50% of cases only and healing occurs in 1 to 3 weeks with variable scarring. [1],[4] The disease may progress to regional lymph nodes leading to large swelling of the submandibular, preauricular axillary, or groin areas and rarely to septicemia. [4]

Cutaneous anthrax, the most common form, is usually curable. On the other hand, the early clinical diagnosis of inhalational anthrax and intestinal anthrax is often diffcult. The outcome of these forms of the disease is usually fatal.

Differential diagnosis and diagnosis

The lesion most commonly confused with cutaneous anthrax (malignant pustule) is vaccinia, which no longer exists. Milkers nodules contracted from the teats of the cow, are characterized by one or several brownish red dome shaped smooth or slightly, papillomatous vegetation (resemble pyogenic granulomas)which are generally confined to the hands and forearms. [4],[16] Orf (ecthtyma contagiosum) is a skin disease found usually in slaughterers or shepherds who may be in contact with sheep suffering from ecthyma contagiosum. A virus causes it and the appearance is more ragged and angry looking compared to the malignant pustule of anthrax. Moreover, Orf lacks the characteristic central eschar. Malignant pustule can be confused with a boil. However, a gram stained smear of the exudate from the lesion usually shows the bacilli if the case is anthrax. A painful pustular eschar in a febrile patient indicates a secondary infection, most often with staphylococcus or streptococcus. [4],[16]

The following clinical features if present are strongly suggestive of cutaneous anthrax. [2],[4]

1. The presence of edema out of proportion to the size of the lesion.

2. Lack of pain during the initial phases of the infection.

3. The rarity of polymorphonuclear leucocytes from vesicular fluid on gram′s stain.

The presence of typical bacilli in the gram′s stained smear from the ulcer and the epidemiological proof may be the only evidence in favor of your diagnosis of cutaneous anthrax, since culture of this organism from skin lesions yields positivity in 60 to 65 per cent of cases only, probably due to prior antibiotic therapy of the microbicidal activity of local antagonistic skin flora. [4]

There have been reports of clinical isolates of B. anthracis that are resistant to penicillin. [24],[25] Because of the potential for drug-resistant strains, including deliberately modified strains, antimicrobial susceptibility testing should be performed on all isolates. Several methods, such as specific enzyme-linked immunosorbent assays, enzyme-linked immunoelectrotransfer blotting and indirect microhemagglutination, have been described for the serologic diagnosis of anthrax. [22] The anthraxin skin test, consisting of subdermal injection of a commercially produced chemical extract of an attenuated strain of B. anthracis, is available for the diagnosis of acute and previous cases of anthrax. [26] New diagnostic techniques focused on the use of the polymerase chain reaction may become useful in the near future, in the clinical setting, where early diagnosis is crucial. [22]

Treatment

Since 20% of untreated cases of cutaneous anthrax develop bacteraemia, which leads to rapid death, energetic treatment with penicillin G is recommended. [1],[4] Penicillin G, 12--24 million IU, is given intravenously daily in six divided does. Ciprofloxacin, erythromycin, tetracycline, and chloramphenicol are alternative drugs for penicillin-senstitive patients. Even if the patient is promptly treated with antimicrobial, cutaneous lesions will continue to progress through the eschar phase [Figure - 3]. In cases of extensive edema, meningitis, or swelling in the head and neck region, corticosteroid therapy should be initiated. [22]

Prevention of anthrax largely depends on the use of vaccines, as the widespread decontamination of contaminated soil is impractical. [4],[20]

Future challenges

A disease of great antiquity, anthrax occupies an important place in the history of infectious diseases because it was the first human disease to be attributed to a specific pathogen. It retains a certain fascination and notoriety partly because of the potential for use of the bacillus spores in biologic warfare. [4],[27]

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