Diagnosis Of Dyspnea And Treatment Of Botulism: A Scientific Review

Differential Diagnosis of Dyspnea

This article by Vasa and his co-authors explaining the course of diagnosis of a 69 year old patient dealing with focal neurogenic distress due to the manifestation of botulism in intricate details. This particular journal was published in the year of 2012 in the renowned New England journal of medicine or NEJM, which is considered to be a source with most valid and authentic research articles belonging to the field of biomedical sciences, with genuine and highly relatable and transferable data (2). The patient under consideration in the assignment was presented in the emergency department due to the symptom of slurred speech and the primary diagnosis had been focal neurologic deficit with the possibility of the cerebro-vascular degeneration and acute stroke. However with the further diagnosis the chance for ischemic stroke causing the bilateral cranial nerve damage was ruled out.

The second possible diagnosis for the patient was the cocaine driven focal neurological deficit that is associated with botulism. Although his physiological and metabolic functions and the lack of normal symptoms associated with the acute cocaine abuse like tachycardia, tremor agitation, diaphoresis had been lacking, hence the option of cocaine intoxication (2).

The presence Ophthalmoplegia and nystagmus showed the probability of the patient having the Wernicke’s encephalopathy owing to his restricted movements and required thiamine administration. Another possible diagnosis for the patient had been the chances for Miller Fisher syndrome, although the normal results of sensory-nerve–conduction studies delimit the chances of demyelinising neuropathy required for Miller Fisher syndrome, and the most plausible diagnosis for the patient was botulism selected as the disease in the final verdict (2).

However, in this context, it has to be mentioned that the most plausible and scientifically reasonable diagnosis was selected as botulism; however the article lacks any clear detail on how the botulism can be treated considering the pr4esent symptoms of the patient and his deteriorating condition (2). This section of the assignment will configure three sets of questions, primary secondary and tertiary, that the article failed to address and will attempt to answer the questions taking assistance from different resources.

Primary question: How can antitoxin therapy treat botulism? 

The first or foremost treatment option for treating the health care concerns like botulism, both food-borne and wound transmitted is the antitoxin therapy. Botulism is caused by the toxin produced by the bacteria Clostridium botulinum, this particular toxin is called botulinum toxin and it is broken down into 8 different variants of neurotoxins. All these neurotoxins work together to block the motor nerve endings of human body from releasing key cytokines like acetylcholine, but are a contributing factor causing flaccid paralysis and the symptoms that the patient was experience is like slurred speech, blurred vision, nausea, vomiting, diarrhea, cramps, and respiratory difficulties (20).

Acetylcholine is a neurotransmitter, latest are responsible factor skating communication between the drain motor neurons and the muscular cells.  The bottling call toxin cost Analysis starts with the facial muscles and then gradually spreads downwards towards the Limbs in case of severe acute botulism, the paralysis of respiratory muscles leads to respiratory failure and life threatening complications (23).

Diagnosis and Treatment of Botulism

The antitoxin therapy and like the inhibitor blocking the action of the bodyline of neurotoxins circulating in the blood. The three neurotoxin variants that are widely established to be the most frequent contributing factor to botulism in humans are considered to be 3 particular neurotoxins, neurotoxin A, B and E. The trivalent antitoxin utilized in the antitoxin therapy for treating botulism prevents the deterioration of botulism disease by blocking the active to means of this neurotoxin and as a result locking the activation of this neurotoxin within the human blood. In case of food borne botulism to remove contaminated formed still inside the gut by using vomiting or enemas.  Heptavalent antitoxin is the patented and certified antitoxin utilized as the antidote in treating food borne botulism.

Secondary question: What Is Antitoxin Therapy?

Therapy is utilized in most of microbe cost in sections that facilitate critical health disorders in humans. Antitoxin can be defined as the antibody with the capability to neutralize and inhibit a specific toxin. Antitoxins are produced within microbial organisms that can be injected into other organisms including human beings (18). Antitoxin therapy Works with the help of passive immunity produced within the body of another organism and helping to treat any infection on health care concern within the body of a completely another organism. Antitoxin therapy has been introduced in the early 1900s, with the use of diphtheria antitoxin for the first time in history to treat diphtheria produced by legendary Emil Adolf Von Behring.

Since that very beginning antitoxin therapy has advanced significantly and now is a common pursuit utilized in the medical science to read the patients of the suffering due to any bacterial infection. Heptavalent botulism antitoxin or HE-BAT, is the most common and licensed commercially available antitoxin effectively used to neutralize all 7 known botulism neurotoxins serotypes (19). This particular antitoxin is derived from the despeciated IgG antibodies with cleaved off Fc protein; however this cleaving process renders the antitoxin a little less efficient in neutralizing the neurotoxin swiftly. Although it also needs to be considered that each ABT is the most effective and broad spectrum Anny talks in that has the ability to work against all non strains of botulism (20).

Tertiary question: What Are the Side Effects of Antitoxin Therapy?

Any treatment procedure treating a critical Health care disorder has its own set of side effects effect in the human body along the way of treating some critical disorder. Antitoxin therapy is the boon to treat bacterial infections causing complicated Health care concerns like botulism. However in spite of the benefits of this therapy there are few side effects associated with the antitoxin therapy utilized in case of botulism as well (22). The side effects associated with Anny talks in therapy utilizing Heptavalent antitoxin includes headache chills fever Rash itching and nausea.  Other than that have talent antitoxin can also triggered allergic reactions and delayed hypersensitivity reactions in the patients that are sensitive to horse proteins (24).

2.Vasa M, Baudendistel TE, Ohikhuare CE, Grace EM, Yan W, Josephson SA, Tierney Jr LM. The Eyes Have It. New England Journal of Medicine. 2012 Sep 6;367(10):938-43.

Antitoxin Therapy for Botulism

20 Naumann M. 149. Clinical comparison of botulinum neurotoxin effects at the neuromuscular junction and autonomic nerves: similarities and differences. Abstracts/Toxicon. 2015;93(S2eS67):S2eS67

23 Scott VL, Villarreal DO, Hutnick NA, Walters JN, Ragwan E, Bdeir K, Yan J, Sardesai NY, Finnefrock AC, Casimiro DR, Weiner DB. DNA vaccines targeting heavy chain C-terminal fragments of Clostridium botulinum neurotoxin serotypes A, B, and E induce potent humoral and cellular immunity and provide protection from lethal toxin challenge. Human vaccines & immunotherapeutics. 2015 Aug 3;11(8):1961-71.

18 Endicott-Yazdani T, Ghazi A, Armstrong D, Guileyardo J, Schuller D. Fatal pulmonary tumor thrombotic microangiopathy caused by undiagnosed metastatic gastric adenocarcinoma. Proceedings (Baylor University. Medical Center). 2015 Oct;28(4):482.

19 Mukherjee J, Dmitriev I, Debatis M, Tremblay JM, Beamer G, Kashentseva EA, Curiel DT, Shoemaker CB. Prolonged prophylactic protection from botulism with a single adenovirus treatment promoting serum expression of a VHH-based antitoxin protein. PloS one. 2014 Aug 29;9(8):e106422.

22 Maslanka SE, Lúquez C, Dykes JK, Tepp WH, Pier CL, Pellett S, Raphael BH, Kalb SR, Barr JR, Rao A, Johnson EA. A novel botulinum neurotoxin, previously reported as serotype H, has a hybrid-like structure with regions of similarity to the structures of serotypes A and F and is neutralized with serotype A antitoxin. Journal of Infectious Diseases. 2015 Jun 10:jiv327

1. Johnson AL, McAdams?Gallagher SC, Aceto H. Outcome of adult horses with botulism treated at a veterinary hospital: 92 cases (1989–2013). Journal of Veterinary Internal Medicine. 2015 Jan 1;29(1):311-9.

In this article addition suffering from dyspnea and her symptoms are evaluated in intricate details to arrive and the most possible and scientifically reasonable diagnosis. In this case a 50 year old woman was admitted to the hospital with the symptoms of fatigue and extreme shortness of breath. The first diagnosis based on the chief symptom is pulmonary disorder. However the additional history of the patient need to the consideration that that is that the patient is exhibiting is not due to pulmonary disorder but is the manifestation of aggressive metastatic breast cancer treated with extensive chemotherapy and thoracic irradiation (3).

With her medical history indicating and the complicated and obstructive treatment for her breast cancer can have an attractive impact on the respiratory Airways of the patient and can have lead to post obstructive pneumonia, along with that methotrexate-induced lung injury or paclitaxel-induced pneumonitis can also be a major cause to the patient suffering with pulmonary distress.

However for other indicates diagnosis of the patients led to the revolution of patient having previous medical history of hypoxemia and having normal breathing sounds is well with helps to narrow down the differential diagnosis to alveolar processes or pleural processes and interstitial processes (3). However the chest radiograph of the patient ruled out all possibilities of the above mentioned complexities and indicated rather at the patient might having a pulmonary vascular disease particularly a pulmonary embolism. Further evidence against any infection in the patient is provided by the normal white cell count coupled with the absence of fever in the patient.

Ultimately the present findings of the patient including hypoxemia and normal chest radiography and nonspecific findings on the chest CT, the chances of the patient having pulmonary thromboembolism is the most. However with a patient having a previous history of underlying cancer the negatives pulmonary angiogram prompted the consideration of the patient having pulmonary tumor thrombotic microangiopathy (3).

This research article discusses in detail the challenges that the physicians face in case of diagnosing and managing pulmonary tumor thrombotic microangiopathy, however there is little to no indication for the therapeutic options and specific Diagnostic procedures for recognizing pulmonary tumor thrombotic microangiopathy. Therefore the second section of this assignment will also configure three sets of questions that are left unanswered in the research article and will attempt to formulate justifiable answer for all those questions.

Primary question: What Are the Diagnostic Challenges for Pulmonary Tumor Thrombotic Microangiopathy?

Pulmonary tumor thrombotic microangiograophy is considered to be one of the most rare complication histological presences of dyspnea and acute pulmonary hypertention. Dyspnea and pulmonary hypertension however are associated symptoms awesome any other pulmonary diseases and health concerns (17).  And moreover display is associated with many other cardiovascular and cerebrovascular health disorders as well along with respiratory disorders. Hence distinguishing pulmonary tumor from Bose take microangiography with any other respiratory or cardiovascular disorder like myocardial infarction or chronic obstructive pulmonary disorder is very difficult. Other than the fact the radio Claus images for pulmonary tumor symbiotic microangiopathic is very similar to ischemic stroke. As mentioned in the research article under evaluation in this assignment, the initial diagnosis for the symptoms of dyspnea and hypertension have been Deemed to be an ischemic stroke (16).  

Moreover it also needs to be mentioned that pulmonary tumor thrombotic microangiopathy is characterized by the presence of microscopic tumor emboli which is very difficult to locate a normal radiograph images. Another important fact associated with this context is that pttm is characterized by rapid detoriation rate and with the constant rate of worsening patient conditions the diagnostic challenges are even more elevated as well (14). The Diagnostic procedures for this particular disease are extremely difficult however PET-CT imaging after the administration of 18F-fluorodeoxyglucose, the diagnosis of pulmonary tumor thrombotic microangiopathy can be considered positive.

Secondary question: what are the characteristics of pulmonary tumor thrombotic microangiopathy?

This particular pulmonary disorder is associated with formation of Coagulation in the vasculaturr causing activation of coagulation and wide spread fibrocellular internal proliferation that leads to blocked pulmonary arteries and arterioles. As a result the vascular resistance is increased multiple folds and it intern facilitates a market elevation in the pulmonary hypertension levels. One of the major symptoms that are associated with pulmonary Soma thrombotic microangiopathy is shortness of breath and pulmonary hypertension. It has to be considered that the blocked Airways are the major reason behind the respiratory distress and which in turn leads to lower oxygen saturation and higher oxygen demand in the body that also brings for fatigue and loss of appetite in the patient (15).

Tertiary question: What Are the Treatment Options for Pulmonary Tumor Thrombotic Microangiopathy?

The treatment option available for PTTM in patients with previous medical history of breast malignancy is anticoagulation therapy. However along with it, enoxaparin administered subcutaneously in a generous concentration, is the also most effectively required for pulmonary tumor thrombotic microangiopathy (14).  A small concentration of dexamethasone is also administered intravenously to the patients suffering with pulmonary tumor thrombotic microangiopathy coupled with a generous dose of warfarin sodium taken orally. Further complications with pulmonary tumor thrombotic microangiopathy can lead to pulmonary hypertension and resultant right ventricular pulmonary overload which in turn can drive the patient towards and myocardial infarction leading to fatal consequences. At this point of deterioration of a patients case of PTTM measures like surgical intervention an appropriate chemotherapy is taken to stabilize the patients worsening condition (13).

1. Gavin MC, Morse D, Partridge AH, Levy BD, Loscalzo J. Breathless. New England Journal of Medicine. 2012 Jan 5;366(1):75-81.
2. Price LC, Wells AU, Wort SJ. Pulmonary tumour thrombotic microangiopathy. Current opinion in pulmonary medicine. 2016 Sep 1;22(5):421-8.
3. Patrignani A, Purcaro A, Calcagnoli F, Mandolesi A, Bearzi I, Ciampani N. Pulmonary tumor thrombotic microangiopathy: the challenge of the antemortem diagnosis. Journal of Cardiovascular Medicine. 2014 Nov 1;15(11):828-33.
4. Toyonaga H, Tsuchiya M, Sakaguchi C, Ajimizu H, Nakanishi Y, Nishiyama S, Morikawa N, Hayashi Y, Nagasaka Y, Yasui H. Pulmonary Tumor Thrombotic Microangiopathy Caused by a Parotid Tumor: Early Antemortem Diagnosis and Long-term Survival. Internal Medicine. 2017 Jan 1;56(1):67-71
5. Uruga H, Fujii T, Kurosaki A, Hanada S, Takaya H, Miyamoto A, Morokawa N, Homma S, Kishi K. Pulmonary tumor thrombotic microangiopathy: a clinical analysis of 30 autopsy cases. Internal Medicine. 2013;52(12):1317-23.

This article focuses on the case study of a 56 year old woman who has been suffering with carpal turner syndrome for 6 months with nodular lesions on the right arm along with increasing tingling and numbness in the arm. The preliminary diagnosis for the patient had been to include infectious, inflammatory or malignant causes (1). However further diversification of the diagnosis including the finding of suppurative granulomas led the direction of the diagnosis to the possibilities of the patient having cutaneous tuberculosis.

The past medical history of the patient also includes taking isoniazid for latent tuberculosis, along with pyridoxine, alprazolam, escitalopram, conjugated estrogen and progestin, and folic acid. However the next set of diagnostic procedures including tuberculin-skin-test along with the previous findings of granulomas indicates ate the possibility of cutaneous mycobacterial infection. The past thorn injury of the patient might have also led to the consequences of the patient having caught a mycobacterial infection, however the chances for the patient getting the chance of having nocardial or fungal contamination like Sporothrix is also possible (4).

At the next phase of the diagnosis has been concerned with a number of lab tests, however the test results do not provide any more details to different between the previous diagnostic possibilities. The repeat biopsy ruled out the possibilities of the patient having cancer. Due to her extensive and increasing pain the MRI imaging of the patient’s right arm showed the presence extensive tenosynovitis in all the tendons of the forearm and a soft-tissue collection around the forearm (1).

The results of her MRI scanning is indicative of the carpal tunnel syndrome due to encasement of nerves by the infectious process. The QuantiFERON–TB Gold testing however negated the chances of the infection being caused by M. tuberculosis and narrowed the diagnosis further down. And following acid-fast bacilli testing indicated positive results for the M. marinum, hence the final diagnosis for the condition that the patient is suffering with is considered to be a cutaneous infection caused by infection of M. marinum leading to encasement of the nerves (1).

This article has explained the diagnostic procedure that is usually undertaken in case of a carpel tunnel syndrome in the patients with a history of cutaneous lesions exceptionally well. The step by step differential diagnosis is deployed very critically giving attention to the minute details of the past medical history and the symptoms exhibited by the patient (1). Hence the detailed information provided by the article needs to be appreciated however, there still are some questions unanswered in the article that a reader can find. This last section of the assignment will configure three questions again, primary secondary and tertiary, and will attempt to string together plausible answers for those questions.

Primary question:  How M. marinum causes cutaneous lesions? 

Mycobacterium marinum is considered to be one of the most common pathogens occurring in various aquatic environments that are known to cause extensive coetaneous infection in the human host. This particular pathogen is known as the most common cause for the human infections, caused as a result of an inoculation of the skin that has been previously abraded or punctured, providing the pathogen with the opportunity to invade the host tissues (5). The wound entry to the pathogen is mostly provided by the fish bite, however in case of the patient under consideration of the article the thorn injury provided the open wound in the patient’s hand. Once inside the human tissues the pathogen is able to escape being phagocytised by macrophages by the means of interrupting the formation of the phagolysosome. The infection begins to manifest as the occurrence of the granuloma or sporotrichotic lymphangitis by rapid sreading due to their actin-based motility (7).

The appearance of the lesions is closer to papules or nodules, often singular or plural. The nodules and papules appear superficial in the preliminary stages and as the infections spreads the lesions become embedded deep into the inner line of tissues. Erythematous plaque is also associated with the lesion formation in this stage, and these lesions can be painful or painless depending on the spread of the infection and can easily become fluctuant as the infection worsens. The size of the lesion also depends on the stage of the infection however the standard size is generally 1–2.5 cm in diameter in the moderately early infection cases. The infection generally takes a substantial period of time to manifest, however in case of patients that are aging or immunologically compromised the spread can take a rapid route (6).

Secondary question: How Mycobacterial Cutaneous Infection Causes Carpel Tunnel Syndrome?

Mycobacterial infections are very common and frequent occurrences as human cutaneus infections, however one caused by the M. marinum is considered a bit rare owing to the restriction of the pathogen to marine habitat. Yet an infection caused by this particular pathogen has become quite common in the current age (8). This kind of infection causes lesions that are deep embedded in the inner line of tissues, and that often can cause superficial nerve damage causing further complications. The patient under consideration in this assignment has been suffering with the symptoms of carpel tunnel syndrome caused by the pressure on the median nerve in the carpel tunnel in the hands (9).

It has to be mentioned in this context that this particular symptom is caused by the nerve entrapment that closes off the sensation to the thumb and other fingers and brings forth the sensation of numbness. This blocking of the tunnel is facilitated by the cutaneous lesions narrowing the tunnels in the hands of the and closing off the neuron transmission in the median nerve that in turn cuts off the sensation giving way to numbness (11).

Tertiary question: What Is the Best Treatment Option for Mycobacterial Lesions?

The best treatment options available for the cutaneous lesions caused by M. marinum can be managed by the antibiotic therapy (10). However in cases where the lesions are embedded too deep surgical intervention can be required. Surgical debridement is the treatment option of choice for the patient and to minimize the carpel tunnel syndrome the patient can take the assistance of occupational therapy and daily administration of NSAID drugs (12).Saint S. Skin Deep. New England Journal of Medicine. 2012 Apr 5;366(14):1336-40

4 Roukens AH, Mendels EJ, Verbeet NL, von dem Borne PA, Nicolae-Cristea AR, Bentvelsen RG, van Doorn R, de Boer MG. Disseminated cutaneous Mycobacterium chelonae infection in a patient with acute myeloid leukemia. InOpen forum infectious diseases 2014 Nov 26 (Vol. 1, No. 3, p. ofu103). Oxford University Press.

5 Berkovic J, Vanchiere JA, Gungor A. Non tuberculous mycobacterial lesion of the parotid gland and facial skin in a 4year old girl: A proposed treatment strategy. American journal of otolaryngology. 2016 Apr 30;37(2):89-94.

6 Kaufmann SH. Immunopathology of mycobacterial diseases. InSeminars in immunopathology 2016 Mar 1 (Vol. 38, No. 2, pp. 135-138). Springer Berlin Heidelberg

7 Marion E, Chauty A, Kempf M, Le Corre Y, Delneste Y, Croue A, Marsollier L, Vincent QB, Abel L, Johnson C, Alcaïs A. Clinical features of spontaneous partial healing during Mycobacterium ulcerans infection. InOpen forum infectious diseases 2016 Jan 1 (Vol. 3, No. 1, p. ofw013). Oxford University Press

8 Gonzalez-Santiago TM, Drage LA. Nontuberculous mycobacteria: skin and soft tissue infections. Dermatologic clinics. 2015 Jul 31;33(3):563-77

9 Rollins II MD, Vanderhooft SL. Benign Skin Lesions. InFundamentals of Pediatric Surgery 2017 (pp. 853-862). Springer International Publishing.

10 Kleopa KA. Carpal tunnel syndrome. Annals of internal medicine. 2015 Sep 1;163(5):ITC1

11 Kilic B, Yucel AS, Yaman C, Catikkas F, Herguner G. Carpal Tunnel Syndrome. Advances in Environmental Biology. 2015 Feb 1:1-3

12 Miyamoto H, Halpern EJ, Kastlunger M, Gabl M, Arora R, Bellmann-Weiler R, Feuchtner GM, Jaschke WR, Klauser AS. Carpal tunnel syndrome: diagnosis by means of median nerve elasticity—improved diagnostic accuracy of US with sonoelastography. Radiology. 2014 Feb;270(2):481-6.]

References: 

1. Safdar N, Abad CL, Kaul DR, Saint S. Skin Deep. New England Journal of Medicine. 2012 Apr 5;366(14):1336-40.
2. Vasa M, Baudendistel TE, Ohikhuare CE, Grace EM, Yan W, Josephson SA, Tierney Jr LM. The Eyes Have It. New England Journal of Medicine. 2012 Sep 6;367(10):938-43.
3. Gavin MC, Morse D, Partridge AH, Levy BD, Loscalzo J. Breathless. New England Journal of Medicine. 2012 Jan 5;366(1):75-81.
4. Roukens AH, Mendels EJ, Verbeet NL, von dem Borne PA, Nicolae-Cristea AR, Bentvelsen RG, van Doorn R, de Boer MG. Disseminated cutaneous Mycobacterium chelonae infection in a patient with acute myeloid leukemia. InOpen forum infectious diseases 2014 Nov 26 (Vol. 1, No. 3, p. ofu103). Oxford University Press.
5. Berkovic J, Vanchiere JA, Gungor A. Non tuberculous mycobacterial lesion of the parotid gland and facial skin in a 4year old girl: A proposed treatment strategy. American journal of otolaryngology. 2016 Apr 30;37(2):89-94.
6. Kaufmann SH. Immunopathology of mycobacterial diseases. InSeminars in immunopathology 2016 Mar 1 (Vol. 38, No. 2, pp. 135-138). Springer Berlin Heidelberg.
7. Marion E, Chauty A, Kempf M, Le Corre Y, Delneste Y, Croue A, Marsollier L, Vincent QB, Abel L, Johnson C, Alcaïs A. Clinical features of spontaneous partial healing during Mycobacterium ulcerans infection. InOpen forum infectious diseases 2016 Jan 1 (Vol. 3, No. 1, p. ofw013). Oxford University Press.
8. Gonzalez-Santiago TM, Drage LA. Nontuberculous mycobacteria: skin and soft tissue infections. Dermatologic clinics. 2015 Jul 31;33(3):563-77.
9. Rollins II MD, Vanderhooft SL. Benign Skin Lesions. InFundamentals of Pediatric Surgery 2017 (pp. 853-862). Springer International Publishing.
10. Kleopa KA. Carpal tunnel syndrome. Annals of internal medicine. 2015 Sep 1;163(5):ITC1-.
11. Kilic B, Yucel AS, Yaman C, Catikkas F, Herguner G. Carpal Tunnel Syndrome. Advances in Environmental Biology. 2015 Feb 1:1-3.
12. Miyamoto H, Halpern EJ, Kastlunger M, Gabl M, Arora R, Bellmann-Weiler R, Feuchtner GM, Jaschke WR, Klauser AS. Carpal tunnel syndrome: diagnosis by means of median nerve elasticity—improved diagnostic accuracy of US with sonoelastography. Radiology. 2014 Feb;270(2):481-6.]
13. Price LC, Wells AU, Wort SJ. Pulmonary tumour thrombotic microangiopathy. Current opinion in pulmonary medicine. 2016 Sep 1;22(5):421-8.
14. Patrignani A, Purcaro A, Calcagnoli F, Mandolesi A, Bearzi I, Ciampani N. Pulmonary tumor thrombotic microangiopathy: the challenge of the antemortem diagnosis. Journal of Cardiovascular Medicine. 2014 Nov 1;15(11):828-33.
15. Toyonaga H, Tsuchiya M, Sakaguchi C, Ajimizu H, Nakanishi Y, Nishiyama S, Morikawa N, Hayashi Y, Nagasaka Y, Yasui H. Pulmonary Tumor Thrombotic Microangiopathy Caused by a Parotid Tumor: Early Antemortem Diagnosis and Long-term Survival. Internal Medicine. 2017 Jan 1;56(1):67-71.
16. Minatsuki S, Miura I, Yao A, Abe H, Muraoka H, Tanaka M, Imamura T, Inaba T, Maki H, Hatano M, Kinugawa K. Platelet-derived growth factor receptor-tyrosine kinase inhibitor, imatinib, is effective for treating pulmonary hypertension induced by pulmonary tumor thrombotic microangiopathy. International heart journal. 2015;56(2):245-8.
17. Uruga H, Fujii T, Kurosaki A, Hanada S, Takaya H, Miyamoto A, Morokawa N, Homma S, Kishi K. Pulmonary tumor thrombotic microangiopathy: a clinical analysis of 30 autopsy cases. Internal Medicine. 2013;52(12):1317-23.
18. Endicott-Yazdani T, Ghazi A, Armstrong D, Guileyardo J, Schuller D. Fatal pulmonary tumor thrombotic microangiopathy caused by undiagnosed metastatic gastric adenocarcinoma. Proceedings (Baylor University. Medical Center). 2015 Oct;28(4):482.
19. Mukherjee J, Dmitriev I, Debatis M, Tremblay JM, Beamer G, Kashentseva EA, Curiel DT, Shoemaker CB. Prolonged prophylactic protection from botulism with a single adenovirus treatment promoting serum expression of a VHH-based antitoxin protein. PloS one. 2014 Aug 29;9(8):e106422.
20. Naumann M. 149. Clinical comparison of botulinum neurotoxin effects at the neuromuscular junction and autonomic nerves: similarities and differences. Abstracts/Toxicon. 2015;93(S2eS67):S2eS67.
21. Fan KL, Wang YL, Chu G, Leung LP. Delayed Antitoxin Treatment of Two Adult Patients with Botulism after Cosmetic Injection of Botulinum Type A Toxin. The Journal of Emergency Medicine. 2016 Dec 31;51(6):677-9.
22. Maslanka SE, Lúquez C, Dykes JK, Tepp WH, Pier CL, Pellett S, Raphael BH, Kalb SR, Barr JR, Rao A, Johnson EA. A novel botulinum neurotoxin, previously reported as serotype H, has a hybrid-like structure with regions of similarity to the structures of serotypes A and F and is neutralized with serotype A antitoxin. Journal of Infectious Diseases. 2015 Jun 10:jiv327.
23. Scott VL, Villarreal DO, Hutnick NA, Walters JN, Ragwan E, Bdeir K, Yan J, Sardesai NY, Finnefrock AC, Casimiro DR, Weiner DB. DNA vaccines targeting heavy chain C-terminal fragments of Clostridium botulinum neurotoxin serotypes A, B, and E induce potent humoral and cellular immunity and provide protection from lethal toxin challenge. Human vaccines & immunotherapeutics. 2015 Aug 3;11(8):1961-71.
24. Johnson AL, McAdams?Gallagher SC, Aceto H. Outcome of adult horses with botulism treated at a veterinary hospital: 92 cases (1989–2013). Journal of Veterinary Internal Medicine. 2015 Jan 1;29(1):311-9.

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