Advances in Infectious Diseases, 2012, 2, 67-71 Published Online September 2012 (
Gastrointestinal Anthrax: A Case and Review of Literature
Ayhan Akbulut1*, Handan Akbulut2, Müge Özgüler1, Nuran İnci3, Şinasi Yalçın4
1Department of Infectious Diseases and Clinical Microbiology, Faculty of Medicine, Firat University, Elazıg, Turkey; 2Department
of Immunology, Faculty of Medicine, Firat University, Elazıg, Turkey; 3Sehit Kamil State Hospital, Gaziantep, Turkey; 4Department
of Ear, Nose and Throat Disorders, Faculty of Medicine, Firat University, Elazıg, Turkey.
Email: *
Received June 2nd, 2012; revised July 3rd, 2012; accepted August 4th, 2012
Anthrax which is caused by Bacillus anthracis is typically a disease of herbivores. Spores existing in the skin, meat,
hair or mouth and nose of animals are transmitted to humans through contact with a break in the skin, consumption of
infected meat or inhalation of spores [1]. Infected uncooked or insufficiently cooked meats cause oropharyngeal and
gastrointestinal system (GIS) anthrax. When this infected materials swallowed anthrax spores may cause lesions from
the oral cavity to the caecum. The diagnosis of gastrointestinal system (GIS) anthrax is difficult due to insidious clinical
progression of the disease and difficulty in the isolation of agent pathogen. Releated symptoms of GIS anthrax are sore
throat, neck swelling, diffuculty swallowing, stomach pain, anoreksia, bloody diarrhea, nause, bloody vomiting and
fever. Supportive and antibiotic treatments are required. Benzylpenicillin, rifampicin, clindamycin, chloramphenicol,
imipenem/cilastatin, or vancomycin can be use for treatment, ciprofloxacin or doxycycline may be added to this treat-
ment for serious cases. To emphasize the necessity of taking precautions, an oropharyngeal and intestinal anthrax case
due to consumption of infected and insufficiently cooked meat is presented below.
Keywords: Bacillus anthracis; Oropharyngeal Disease; Gastrointestinal System; Anthrax; Consumption of Infected
1. Case
Forty-two year-old female patient, presenting with swell-
ing which initiated on the right side of the neck and spread
all around the neck and chest, difficulty in swallowing
and breathing, chills and fever symptoms, referred to the
emergency department and hospitalized for evaluation.
Detailed history of the patient revealed that she lived
in the countryside, dealed with livestock farming and two
days before the swelling appeared, she cooked and ate
the meat of an animal which was designated as ill by
veterinary surgeon.
In the initial examination, general status is regarded as
intermediate, axillary temperature 37.8˚C, heart beat 76/
min and arterial blood pressure was measured as 110/60
mmHg. Painless oedema was observed all over the neck,
being more prominent on the right side and also on the
upper 1/3 region of the chest. During palpation, a number
of lymph nodes were detected but the dimension of
lymphadenopathy (LAP) could not be determined because
of oedema. In the pharyngeal examination, a mass re-
sembling an abscess with darker color in the center and
intirely covering the posterior wall of the pharynx was
observed (Figure 1(a)).
The findings of the initial laboratory evaluation of the
patient are as follows: in whole blood cell count, white
blood cells (WBC) 13,300/mm3 with differential count of
polimorphonuclear WBC (PNL) 86%, lymphocytes 7.4%,
monocytes 6.6%; hemoglobin 11.5 gr/dL, hematocrit 34.9%;
platelet count 144.000/mm3; red blood cell (RBC) sedi-
mantation rate (ESR) 13 mm/hr; C-reactive protein (CRP)
24 mg/L. Transaminase values were detected as AST 32
IU/L and ALT 12 IU/L, urea as 67 mg/dL, creatinine as
1.3 mg/dL; the other biochemical and urine analysis val-
ues were found to be within normal limits.
Emergency neck computerized tomography showed a
lobulated mass compatible with abscess, with approximate
dimensions of 3 × 2.5 × 4 cm according to peripheral and
internal septal contrast and constricting the trachea.
Multipl LAPs with conglomerated apperance and largest
with a dimension of 3.2 cm were detected in the right
submandibular, sublingual and cervical regions. On the
right side of the neck, subdermal soft tissue with oede-
matous appearance was observed (Figure 2(a)). The de-
tails of the radiologic findings of this case were descri-
bed previously [2].
Two blood cultures and culture from the wound were
performed. Bacillus anthracis was grown in the pharyn-
geal culture of the patient. The patient was pre-diagnosed
*Corresponding author.
Copyright © 2012 SciRes. AID
Gastrointestinal Anthrax: A Case and Review of Literature
as having oropharyngeal anthrax and placed on a daily
treatment of intravenous 24 million units penisilin G (6 ×
4 million units) and 500 mg levofloxacin. Due to dispnea,
dexametason 8 mg i.v. and cold steam were added to
On the second day of hospitalization, oedema on the
neck and chest started to recover and ecchymosis deve-
loped in the same region (Figure 1(c)). Airway passage
was evaluated on a daily basis. Passage was observed to
be relieved in due course.
On the 4th day of treatment, general status of the
patient was good and passage improved considerably.
Repeat whole blood cell count results were as follows:
white blood cells 9200/mm3; hemoglobin 11.0 gr/dL, he-
matocrit 32.6%; platelet count 187.300/mm3; ESR 12
Observations of day 6 were significant recovery of the
abscess and improvement in respiration; the only symp-
tom observed was dysphagia (Figure 1(b)). Unfortuna-
tely, even though the patient was adviced not to touch the
abscess, her husband informed healthcare personnel that
she popped up the abscess with her finger. Upon interview
of the patient, she admitted that she popped up the
abscess with her finger and swallowed the draining fluid.
On the 8th day of treatment, the patient presented with
bloody defecation 4 times in a day; following findings
were observed at this stage: axillary temperature 37.0˚C,
heart rate 105 /min, arterial blood pressure 130/80 mmHg,
pallor of skin and sclera, abdominal distention, diminishing
intestinal tones, voluntary resistance and tenderness upon
palpation. Melena was observed in rectal touch exami-
nation. Following findings were determined in the labo-
ratory evaluation: in whole blood cell count, white blood
cell count 23,600/mm3 ( PNL 88%, lymphocyte 12%, mo-
nocyte 1.2%); hemoglobin 7.2 gr/dL, hematocrit 20.5%;
platelets 115.000/mm3.
Transaminase values of AST 83 IU/L, ALT 51 IU/L,
LDH: 935 IU/L, GGT: 23 IU/L, total bilirubin: 1.3 mg/
dL, direct bilirubin: 0.30 mg/dL, total protein: 3.4 mg/dL,
albumin: 1.87 mg/dL, urea: 48 mg/dL, creatinine: 1.5 mg/
dL, Na: 134 mmol/L and calcium: 6.2 mg/dL were de-
tected. Feces was dark brown, loose, unformed and bloody
with no mucus. Microbiological evaluation of the feces
revealed a large number of red blood cells and 1 - 2
white blood cells in certain regions. No parasite, parasite
egg, cyst or trophozoid was detected. Blood culture was
repeated three times at half hour intervals.
Oral nutrition of the patient was discontinued and GIS
bleeding protocol was initiated. Supportive therapy and
blood transfusion was administered. Emergency abdominal
ultrasound (USG) examination showed disseminated and
abundant fluid around perihepatic, perisplenic and in-
testinal loops. Oedematous intestinal loops in the lower
abdominal quadrant and fluid in bilateral hemithorax
were detected. Upon these USG findings, the patient was
evaluated by general surgery department and diagnosed
with GIS bleeding. Paracentesis was performed for the
fluid in the abdominal cavity; the characteristics of para-
centesis fluid was transuda and on microscobic exami-
nation, abundant red blood cells (380 hücre/mm3) were
Endoscopic examination of oesophagus, gastrum and
small intestines was not performed due to oropharyngeal
abscess. Emergency colonoscopic examination revealed
multiple ulcers in the colon. Biopsy was performed from
these ulcers. Even though no bleeding focus was observed
in the lumen of the colon, the content of colon was bloody.
In the computerized tomographic angiography of the
patient, contrast material leakage was detected around
regions covered by superior mesenteric artery (Figure
2(b)). Surgical intervention was deferred on the basis of
patient’s melena, oedema of small intestine and fluid
collection between intestinal loops, presence of ulcers in
colon and deterioration of general status of the patient.
Blood transfusion, fresh frozen plasma, platelet sus-
pension and albumin replacement were administered to
the patient whose hemoglobin, hematocrit and platelet
values decreased continuously. Unfortunately, deterioration
of general status persisted. Following bleeding symptoms,
a septic state developed with signs of tachycardia, hy-
potension and tachypnea. Bacillus anthracis grew on two
concurrent blood cultures (Fgiure 1(d)). Patient deceased
on the 17th day of penicillin G and levofloxacin treat-
2. Discussion
Bacillus anthracis is a Gram (+), spore-forming, encaps-
ulated and non-motile bacteria. Spores may be located
centrally or paracentrally and do not cause dilatation in
the bacteria dimentions [1-4].
Around 90% - 95% of anthrax infections are cutaneous
infections due to easy transmission. Transmission by
inhalation causes pulmonary anthrax and oral transmission
leads to gastrointestinal anthrax. Rate of sepsis following
internal organ anthrax infections is extremely high.
Gastrointestinal anthrax frequently causes multiple and
superficial ulcers all along gastrointestinal tract starting
from oral cavity to caecum; in some cases, ulcers may
also be seen in the colon . Massive and fatal bleeding is
seen in serious cases of ulcerative lesions [1-4].
When Bacillus anthracis spores are ingested orally, they
attach to the epithelial cells of tonsilla and M cells over the
payer plaques of small intestine. Live bacteriae releases a
toxin while it reproduces. The disease presents a wide spec-
trum of states ranging from subclinic infection to death.
The exact infectious dose in humans is not known but
for oral anthrax, the determined minimal infectious dose
(Mid50) 50 mg is approximately 1011 spores [5].
Copyright © 2012 SciRes. AID
Gastrointestinal Anthrax: A Case and Review of Literature
Copyright © 2012 SciRes. AID
(a) (b)
(c) (d)
Figure 1. (a) Abscess of anthrax oroferangeal; (b) The observed bleeding after anthrax abscess decrease; (c) Were reduced
after drenation abscess oroferangeal of anthrax; (d) Gram stained preparations of the Bacillus anthracis in the blood culture
(a) (b)
Figure 2. (a) In contrast CT: cervical region and in multiple necrotic LAPs in that are contrast. Right to be more specific with
soft tissue edema in the air passages provided in the plan from the recession is being monitored; (b) The common areas in the
region prevertebral cervical fluid (hemorrhagic exudative) increase.
Clinical findings in oropharyngeal anthrax includes
fever, inflammatory lesions in the oral cavity or oropha-
rynx, oedema and lymphadenopathy in the neck; the mor-
tality rate of the disease is high [1]. Oropharyngeal anthrax
should be differentiated from diphteria, complicated ton-
sillitis, streptococcal pharyngitis, vincent angina, ludwing
Gastrointestinal Anthrax: A Case and Review of Literature
angina, parapharyngeal abscess and deep neck abscess [6].
Ulcerative lesions of gastrointestinal (GIS) anthrax are
usually more than one and superficial. Lesions located in
gastrum, oesophagus and jejunum may cause fatal mas-
sive bleeding. In addition, these lesions may lead to ob-
struction [7-10], perforation or various combinations of
these complications. GIS anthrax may cause ascites. In
some cases, dehydration from the vascular compartment
may cause shock and fatality [10-15].
Intestinal anthrax presents with three clinical phases:
Phase I: includes fainting, asthenia, mild fever and
headache. Patients are rarely treated at this stage because
of few symptoms. In a small number of patients, rash on
the face or redness of the conjunctiva may be seen.
Phase II: starts in 24 hours and abdominal pain is
added to symptoms. Abdominal pain, which is initially
mild, intensifies and adopts a continuous course. Mild
fever, nausea and vomiting is seen frequently; diarrhea, if
present, is mild. On physical examination, mass and ab-
dominal distension is detected in right lower quadrant
and periumblical area.
Phase III: there is a persistent and rapidly intensifying
abdominal pain and in most cases, GIS bleeding develops.
In patients where laparotomy is performed, abundant and
viscous, yellow fluid, hypertrophic mesenteric lymph
nodes especially in the ileocaekal area (3 - 5 cm) and
oedema in some parts of the small intestine, caekum and
ascending colon is observed. In case of failure on sur-
gical removal of the diseased part, a transient recovery is
seen. In these patients, ascites develops again and most
of the patients are lost, due to shock states [16].
During surgery and in autopsy series, small red nodules
(0.5 - 1 cm) with surrounded necrotic centers (2 - 3 cm)
are seen in hemorrhagic areas surrounded by oedema in
the intestinal wall [17].
GIS anthrax should be differentiated from causes lead-
ing to early acute abdominal syndrome as well as Clostri-
dium perfiringens which causes necrotizing enteritis and
other bacterial or parasite agents which lead to bloody
There are few literature review and case reports. Most
of the this case reports and releated articles about GIS
anthrax says that, this disease is very dangerous and its
mortality rates 25% - 60%. Death due to GIS anthrax is
reported to occur in 2 - 5 days [2,7,8,19-21].
In our case, the patient presented with oropharyngeal
anthrax. We suspected oropharyngeal anthrax with patient’
s epidemiological history. Then we recieved blood and
wound cultures and B. anthracis investigated at this cul-
tures. Computerized tomography (CT) used for diagnosis
and oropharyngeal abcess detected at CT images. On the
6th day of treatment, her general status improved and the
abscess in the pharynx showed considerable decrease.
The patient drained the abscess with her own finger and
consequently caused GIS anthrax. Since the patient pre-
sented with dysphagia, it was not possible to give oral
contrast material and therefore, abdominal computerized
tomography with contrast material could not be performed;
as a result, it could not be confirmed whether she had or
did not have GIS anthrax initially. Nevertheless, absence of
abdominal pain, diarrhea and vomiting in the beginning,
improvement of general status in 7 days and her own
statement on draining the abscess with her finger and
swallowing the fluid lead us to conclude that GIS anthrax
developed later on.
In Turkey, anthrax is reported to show an endemic
course with 96.9% of the cases presenting with cutaneous
anthrax [18-21]. In an investigation, oropharyngeal anthrax
is seen in 7 cases and intestinal anthrax is diagnosed in 1
case [19]. In Turkey, no resistance was observed against
penicillin G for Bacillus anthracis; therefore, penicillin G
is the treatment of choice as an effective agent. It has been
reported that aminoglycoside, together with penicillin G is
more effective in oropharyngeal or intestinal anthrax [18-
21]. In our case, aminoglycoside was not preferred as an
adjunctive antimicrobial because creatinine levels of the
patient were high (creatinine: 1.3 - 1.5 mg/dL). Even though
the usual treatment period is indicated as 10 - 14 days, due
to insufficient improvement in our patient, treatment was
not terminated.
In conclusion, due to the high mortality rates of GIS
antrax must be prevented. In countries which are endemic
anthrax areas, carving and eating the meat of sick animals
should absolutely be prevented plus people should be in-
formed and warned to take precautions about the disease.
Besides, in cases of oropharyngeal abscesses, anthrax
should be considered and a careful patient history should
be taken, laboratories should be warned under suspicious
conditions and necessary evaluations should be performed.
We should approach oropharyngeal anthrax cases care-
fully, taking into account intestinal anthrax cases.
[1] M. Neguţ and D. M. Caplan, “Epidemiology Studies Re-
garding Anthrax Epidemic in Romania,” Bacteriologia,
Virusologia, Parazitologia, Epidemiologia, Vol. 47, No.
3-4, 2002, pp. 161-165.
[2] H. Ozdemir, K. Demirdag, T. Ozturk and E. Kocakoc,
“Anthrax of the Gastrointestinal Tract and Oropharynx:
CT Findings,” Emergency Radiology, Vol. 17, No. 2, 2010,
pp. 161-164. doi:10.1007/s10140-009-0821-y
[3] C. Kunanusont, K. Limpakarnjanarat and J. M. Foy, “Out-
break of Anthrax in Thailand,” Annals of Tropical Medi-
cine and Parasitology, Vol. 84, No. 5, 1990, pp. 507-512.
[4] D. P. Perl and J. R. Dooley, “Anthrax,” In: C. H. Binford
and D. H. Connor, Eds., Pathology of Tropical and Ex-
traordinary Diseases, Armed Forces Institute of Pathology,
Washington DC, 1976, pp. 118-123.
Copyright © 2012 SciRes. AID
Gastrointestinal Anthrax: A Case and Review of Literature
Copyright © 2012 SciRes. AID
[5] Z. A. Kanafani, A. Ghossain, A. I. Sharara, J. M. Hatem and
S. S. Kanj, “Endemic Gastrointestinal Anthrax in 1960s
Lebanon: Clinical Manifestations and Surgical Findings,”
Emerging Infectious Diseases, Vol. 9, No. 5, 2003, pp. 520-
525. doi:10.3201/eid0905.020537
[6] WHO, “Antrax in Humans and Animals,” 4th Edition,
WHO Press, Geneva, 2008.
[7] T. Tantajumroon and K. Panas-Ampol, “Intestinal Anthrax:
Report of Two Cases,” Journal of The Medical Associa-
tion of Thailand, Vol. 51, 1968, pp. 477-480.
[8] T. Tantachumroon, “Pathologic Studies of İntestinal Anthrax:
Report of 2 Cases,” Chiang Mai Medical Bulletin, Vol. 4,
1966, pp. 135-144.
[9] E. Kohout, A. Sehat and A. M. Ashraf, “Anthrax: A Con-
tinuous Problem in Southwest Iran,” The American Jour-
nal of the Medical Sciences, Vol. 247, No. 3, 1964, pp.
565-575. doi:10.1097/00000441-196405000-00006
[10] G. P. Jena, “Intestinal Anthrax in Man: A Case Report,”
Central African Journal of Medicine, Vol. 26, No. 12,
1980, pp. 253-254.
[11] Centers for Disease Control and Prevention (CDC), “Gas-
trointestinal Anthrax after an Animal-Hide Drumming
Event—New Hampshire and Massachusetts, 2009,” Mor-
bidity and Mortality Weekly Report, Vol. 59, No. 28, 2010,
pp. 872-877.
[12] P. Baht, D. N. Mohan and H. Srinivasa, “Intestinal An-
thrax with Bacteriological İnvestigations,” The Journal of
Infectious Diseases, Vol. 152, No. 6, 1985, pp. 1357-1358.
[13] W. Dutz, F. Saidi and E. Kohout, “Gastric Anthrax with
Massive Ascites,” Gut, Vol. 11, No. 4, 1970, pp. 352-354.
[14] A. Alizad, E. M. Ayoub and N. Makki, “Intestinal Anthrax
in a Two-Year-Old Child,” The Pediatric Infectious Di-
sease Journal, Vol. 14, No. 5, 1995, pp. 394-395.
[15] T. Sirisanthana, U. Jesadaporn, “Survival of a Patient with
Gastrointestinal Anthrax,” Chiang Mai Medical Bulletin,
Vol. 24, No. 1, 1985,pp. 1-5.
[16] D. R. Nalin, B. Sultana, R. Sahunja, A. K. Islam, M. A.
Rahim, M. Islam, et al., “Survival of a Patient with Intes-
tinal Anthrax,” American Journal of Medicine, Vol. 62,
No. 1, 1977, pp. 130-132.
[17] A. Ghossain, “Intestinal Anthrax,” In: T. S. Harrison, Ed.,
Surgery for All: A View from the Developing World,
Ferozsons, Lahore, 1992, pp. 144-150.
[18] S. Felek, A. Akbulut and A. Kalkan, “A Case of Antrax
Sepsis: Non Fatal Course,” Journal of Infection, Vol. 38,
No. 3, 1999, pp. 201-202.
[19] M. Doganay, A. Almaç and R. Hanağasi, “Primary Throat
Anthrax. A Report of Six Cases,” Scandinavian Journal
of Infectious Diseases, Vol. 18, No. 5, 1986, pp. 415-419.
[20] M. Doganay and G. Metan, “Human Anthrax in Turkey
from 1990 to 2007,” Vector-Borne and Zoonotic Diseases,
Vol. 9, No. 2, 2009, pp. 131-140.
[21] M. Doganay, “Ingestional (Oral Route/Enteric) Antrax: Is
It Problem in Turkey?” Flora, Vol. 14, No. 3, 2009, pp.