Anthrax natural history, complications and prognosis: Difference between revisions
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===Inhalation Anthrax=== | ===Inhalation Anthrax=== | ||
The term “Inhalation anthrax” has largely replaced the older names for this form of the disease, the most common of which was “pulmonary anthrax”, reflecting the fact that active infection occurs in the lymph nodes, rather than the lung itself, and that bronchopneumonia does not occur. The inhaled spores are carried by macrophages from the lungs, where there is no overt infection, to the lymphatic system where the infection progresses. Germination and initial multiplication begin within the | The term “Inhalation anthrax” has largely replaced the older names for this form of the disease, the most common of which was “pulmonary anthrax”, reflecting the fact that active infection occurs in the lymph nodes, rather than the lung itself, and that bronchopneumonia does not occur. The inhaled spores are carried by macrophages from the lungs, where there is no overt infection, to the lymphatic system where the infection progresses. Germination and initial multiplication begin within the macrophages while in transit to the lymph nodes. The vegetative cells kill the macrophages and are released into the bloodstream where they continue to multiply and lead to fatal septicemia. | ||
Symptoms prior to the onset of the final | Symptoms prior to the onset of the final hyperacute phase are nonspecific, and suspicion of anthrax depends on the knowledge of the patient’s history. | ||
The mild initial phase of nonspecific symptoms is followed by the sudden development of dyspnoea, cyanosis, disorientation with coma, and death. | |||
The typical clinical course of this form of the disease is consistent with the lesion development within the mediastinal lymph nodes before the development of bacteraemia. The assault on the lung appears to be two-pronged. In the initial phase, the blockade of the lymphatic vessels develops, in association with symptoms such as a sensation of tightness of the chest. Lymphatic stasis is associated with oedema, which may be apparent above the thoracic inlet, and pleural effusion. Histological sections of the lung may reveal bacilli within the lymphatic vessels. In the acute phase, damage associated with sep-ticaemia occurs. | |||
Lymphatic stasis resulting from the damaged lymph nodes leads to dilatation of pulmonary lymphatics which originate in the pleura and drain towards the hilum, following interlobular septa in association with blood vessels. The stasis manifests as an early onset pleural effusion and peripheral infiltrates, representing thickened bronchovascular bundles, detectable on chest X-ray. These findings mark fully developed initial stage illness. ultimately, the bacteria escape from the damaged lymph nodes and invade the blood stream via the thoracic duct. once the bacteraemia and associated toxaemia reach a critical level, the severe symptoms characteristic of the acute phase illness are manifest. During the acute phase illness, damage of the lung tissue becomes apparent on X-ray. this damage results from the action of anthrax toxin on the endothelium of the lung’s capillary bed (dalldorf et al., 1971). Primary damage of the lung is not normally a feature of the initial phase illness and primary pulmonary infection is an uncommon presentation. | |||
===Gastrointestinal Anthrax=== | ===Gastrointestinal Anthrax=== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]
Overview
Natural History
Cutaneous Anthrax
Anthrax eschars are generally seen on exposed unprotected regions of the body, mostly on the face, neck, hands and wrists. Generally cutaneous lesions are single, but sometimes two or more lesions are present. For example, with infection resulting from skinning an infected dead animal, multiple lesions may be seen on hands, wrists or arms.
The incubation period ranges from as little as 9 hours to 3 weeks, mostly 2 to 6 or 7 days.
The general scenario is as follows:
- Day 0 entry of the infecting B. anthracis (usually as spores) through a skin lesion (cut, abrasion, etc.) or (possibly as vegetative forms or vegetative forms and spores) by means of a fly-bite.
- Days 2-3 A small pimple or papule appears.
- Days 3–4 A ring of vesicles develops around the papule. Vesicular fluid may be exuded. Unless the patient was treated, capsulated B. anthracis can be identified in appropriately stained smears of this fluid, and the bacterium can be isolated by culture. Marked oedema starts to develop. Unless there is secondary infection, there is no pus and pathognomonically the lesion itself is not painful, although painful lymphadenitis may occur in the regional lymph nodes and a feeling of pressure may result from the oedema. The lesion is usually 1–3 cm in diameter and remains round and regular. Occasionally a lesion may be larger and irregularly shaped.
- Days 5–7 the original papule ulcerates to form the characteristic eschar. topical swabs will not pick up B. anthracis. Detection in smears or by culture requires lifting the edge of the eschar with tweezers (this gives no pain unless there is secondary infection) and obtaining fluid from underneath. The fluid will probably be sterile if the patient has been treated with an antibiotic. Edema extends some distance from the lesion. Systemic symptoms are low-grade fever, malaise and headache. If the cutaneous reaction is more severe, especially if located on the face, neck or chest, clinical symptoms may be more severe with more extensive edema extending from the lesion, toxamia, a change in mental status, high fever, hypotension, regional lymphadenomegaly and the patient unable to eat or drink. Tracheotomy is a life-saving procedure in patients having a cutaneous lesion on the face or neck with an extensive oedema leading to compression on the trachea. this clini- cal manifestation is very dangerous (doganay et al., 1987; doganay, 1990).
- Day 10 the eschar begins to resolve; resolution takes several weeks and is not hastened by treatment. Clinicians unaware of this suffer from concern that the treatment has been inef- fective. A small proportion of untreated cases develop sepsis or meningitis with hyperacute symptoms.
Time to resolution will depend on the size, location and local severity of the lesion. The initial crust separates several weeks after onset, with subsequent healing by granulation. Sometimes the separation of the crust is delayed and the lesion may become secondarily infected. In this situation, the crust should be excised surgically. Lesions characterized by “malignant edema” can be expected to take months to heal. Very large lesions may require skin grafts, and lesions in locations such as the eyelid may require surgical intervention due to scarring.
Inhalation Anthrax
The term “Inhalation anthrax” has largely replaced the older names for this form of the disease, the most common of which was “pulmonary anthrax”, reflecting the fact that active infection occurs in the lymph nodes, rather than the lung itself, and that bronchopneumonia does not occur. The inhaled spores are carried by macrophages from the lungs, where there is no overt infection, to the lymphatic system where the infection progresses. Germination and initial multiplication begin within the macrophages while in transit to the lymph nodes. The vegetative cells kill the macrophages and are released into the bloodstream where they continue to multiply and lead to fatal septicemia.
Symptoms prior to the onset of the final hyperacute phase are nonspecific, and suspicion of anthrax depends on the knowledge of the patient’s history.
The mild initial phase of nonspecific symptoms is followed by the sudden development of dyspnoea, cyanosis, disorientation with coma, and death.
The typical clinical course of this form of the disease is consistent with the lesion development within the mediastinal lymph nodes before the development of bacteraemia. The assault on the lung appears to be two-pronged. In the initial phase, the blockade of the lymphatic vessels develops, in association with symptoms such as a sensation of tightness of the chest. Lymphatic stasis is associated with oedema, which may be apparent above the thoracic inlet, and pleural effusion. Histological sections of the lung may reveal bacilli within the lymphatic vessels. In the acute phase, damage associated with sep-ticaemia occurs.
Lymphatic stasis resulting from the damaged lymph nodes leads to dilatation of pulmonary lymphatics which originate in the pleura and drain towards the hilum, following interlobular septa in association with blood vessels. The stasis manifests as an early onset pleural effusion and peripheral infiltrates, representing thickened bronchovascular bundles, detectable on chest X-ray. These findings mark fully developed initial stage illness. ultimately, the bacteria escape from the damaged lymph nodes and invade the blood stream via the thoracic duct. once the bacteraemia and associated toxaemia reach a critical level, the severe symptoms characteristic of the acute phase illness are manifest. During the acute phase illness, damage of the lung tissue becomes apparent on X-ray. this damage results from the action of anthrax toxin on the endothelium of the lung’s capillary bed (dalldorf et al., 1971). Primary damage of the lung is not normally a feature of the initial phase illness and primary pulmonary infection is an uncommon presentation.
Gastrointestinal Anthrax
Complications
Prognosis
The anthrax prognosis will depend on a number of factors, including:
- The type of anthrax
- How early the anthrax is diagnosed
- The strain of anthrax bacteria
- The patient's age and health condition