Anthrax natural history, complications and prognosis: Difference between revisions
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* 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. | * 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. | 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 macro- phages while in transit to the lymph nodes (hanna & ireland, 1999). the vegetative cells kill the macro- phages and are released into the bloodstream where they continue to multiply and lead to fatal septicae- mia (see also section 5.2). | |||
Symptoms prior to the onset of the final hypera- cute phase are nonspecific, and suspicion of anthrax depends on the knowledge of the patient’s history. Analysis of 10 of the 11 inhalational cases associated with the anthrax letter events of 2001 in the uSA (Jernigan et al., 2001; inglesby et al., 2002) revealed a median incubation period of 4 days (range 4–6 days) and a variety of symptoms at initial presentation including fever or chills (n=10), sweats (n=7), fatigue or malaise (n=10), minimal or nonproductive cough (n=9), dyspnoea (n=8), changes in mental state including confusion (n=5) and nausea or vomiting (n=9). All patients had abnormal chest X-rays with infiltrates (n=7), pleural effusion (n=8) and medias- tinal widening (n=7). Mediastinal lymphadenopathy was present in seven cases. in the previously best– documented set of five case reports of inhalational anthrax, Plotkin et al. (1960) also recorded headache, | |||
muscle aches and development of a cough in four patients and mild pain in the chest in one. Jernigan et al. (2001) drew attention to profound sweating as a prominent feature in their patients not emphasized in previous reports. | |||
in contrast to the median incubation period of 4 days found in the anthrax letter inhalation cases, Brookmeyer et al. (2001) estimated it to have been 11 days in the Sverdlovsk outbreak. one considera- tion that should be kept in mind is the possibility that reflux of spores from the respiratory tract into the alimentary tract may occur with the develop- ment of lesions there, and that this may affect time of onset of symptoms. however, while high exposure may lead to swallowing as well as inhaling spores, it is the alternative view that enteric manifestations result from toxic action being carried to the gas- trointestinal tract via the bloodstream rather than from concurrent ingestion anthrax. | |||
the mild initial phase of nonspecific symptoms is followed by the sudden development of dyspnoea, cyanosis, disorientation with coma, and death. in Plotkin et al.’s cases, treatment was unsuccessful in four of the patients, and death occurred within 24 hours of onset of the hyperacute phase. | |||
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 asso- ciation with symptoms such as a sensation of tight- ness 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 ves- sels. in the acute phase, damage associated with sep- ticaemia occurs. this is manifested morphologically by the changes described by dalldorf et al. (1971). occasional patients do not develop the mediastini- tis which usually typifies this form of the disease. Mediastinal widening has been found to be a rela- tively frequent manifestation of other diseases, lead- ing to the recommendation for computerized axial tomography (CAt) scans to demonstrate lymph node involvement. | |||
recent findings using computerized tomography (Ct) scans combined with autopsy observations have enhanced clinical interpretation of early inhalational anthrax evolution (Galvin et al., 2001). the earliest detectable specific finding pointing to inhalational anthrax is mediastinal widening on posteroanterior (PA) chest X-rays. however, mediastinal widening is not a rare finding in a series of patients present- ing at a hospital emergency department. imaging in inhalational anthrax patients using a non-contrast spiral Ct will reveal hyperdense lymph nodes in the mediastinum associated with oedema of mediastinal fat. the hyperdensity of the lymph nodes represents haemorrhage and necrosis, following spore germina- tion and vegetative growth with exotoxin elaboration. 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, represent- ing 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 pres- entation (see also section 5.2). | |||
the X-ray picture of the lung appears to be a very sensitive diagnostic aid with multiple abnormali- ties, including mediastinal widening, paratracheal fullness, pleural effusions, parenchymal infiltrates and mediastinal lymphadenopathy (Jernigan et al., 2001). | |||
As stated in section 4.4.1, the number of recorded cases of inhalational anthrax in history is lower than might be perceived from the high profile given to this manifestation, and it has long been suspected, with some supportive evidence, that undiagnosed low-grade inhalational infections with recovery may occur in at-risk occupations. | |||
===Gastrointestinal Anthrax=== | |||
==Complications== | ==Complications== | ||
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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 macro- phages while in transit to the lymph nodes (hanna & ireland, 1999). the vegetative cells kill the macro- phages and are released into the bloodstream where they continue to multiply and lead to fatal septicae- mia (see also section 5.2).
Symptoms prior to the onset of the final hypera- cute phase are nonspecific, and suspicion of anthrax depends on the knowledge of the patient’s history. Analysis of 10 of the 11 inhalational cases associated with the anthrax letter events of 2001 in the uSA (Jernigan et al., 2001; inglesby et al., 2002) revealed a median incubation period of 4 days (range 4–6 days) and a variety of symptoms at initial presentation including fever or chills (n=10), sweats (n=7), fatigue or malaise (n=10), minimal or nonproductive cough (n=9), dyspnoea (n=8), changes in mental state including confusion (n=5) and nausea or vomiting (n=9). All patients had abnormal chest X-rays with infiltrates (n=7), pleural effusion (n=8) and medias- tinal widening (n=7). Mediastinal lymphadenopathy was present in seven cases. in the previously best– documented set of five case reports of inhalational anthrax, Plotkin et al. (1960) also recorded headache,
muscle aches and development of a cough in four patients and mild pain in the chest in one. Jernigan et al. (2001) drew attention to profound sweating as a prominent feature in their patients not emphasized in previous reports.
in contrast to the median incubation period of 4 days found in the anthrax letter inhalation cases, Brookmeyer et al. (2001) estimated it to have been 11 days in the Sverdlovsk outbreak. one considera- tion that should be kept in mind is the possibility that reflux of spores from the respiratory tract into the alimentary tract may occur with the develop- ment of lesions there, and that this may affect time of onset of symptoms. however, while high exposure may lead to swallowing as well as inhaling spores, it is the alternative view that enteric manifestations result from toxic action being carried to the gas- trointestinal tract via the bloodstream rather than from concurrent ingestion anthrax.
the mild initial phase of nonspecific symptoms is followed by the sudden development of dyspnoea, cyanosis, disorientation with coma, and death. in Plotkin et al.’s cases, treatment was unsuccessful in four of the patients, and death occurred within 24 hours of onset of the hyperacute phase.
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 asso- ciation with symptoms such as a sensation of tight- ness 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 ves- sels. in the acute phase, damage associated with sep- ticaemia occurs. this is manifested morphologically by the changes described by dalldorf et al. (1971). occasional patients do not develop the mediastini- tis which usually typifies this form of the disease. Mediastinal widening has been found to be a rela- tively frequent manifestation of other diseases, lead- ing to the recommendation for computerized axial tomography (CAt) scans to demonstrate lymph node involvement.
recent findings using computerized tomography (Ct) scans combined with autopsy observations have enhanced clinical interpretation of early inhalational anthrax evolution (Galvin et al., 2001). the earliest detectable specific finding pointing to inhalational anthrax is mediastinal widening on posteroanterior (PA) chest X-rays. however, mediastinal widening is not a rare finding in a series of patients present- ing at a hospital emergency department. imaging in inhalational anthrax patients using a non-contrast spiral Ct will reveal hyperdense lymph nodes in the mediastinum associated with oedema of mediastinal fat. the hyperdensity of the lymph nodes represents haemorrhage and necrosis, following spore germina- tion and vegetative growth with exotoxin elaboration. 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, represent- ing 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 pres- entation (see also section 5.2).
the X-ray picture of the lung appears to be a very sensitive diagnostic aid with multiple abnormali- ties, including mediastinal widening, paratracheal fullness, pleural effusions, parenchymal infiltrates and mediastinal lymphadenopathy (Jernigan et al., 2001).
As stated in section 4.4.1, the number of recorded cases of inhalational anthrax in history is lower than might be perceived from the high profile given to this manifestation, and it has long been suspected, with some supportive evidence, that undiagnosed low-grade inhalational infections with recovery may occur in at-risk occupations.
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