1. Typhoid fever is caused by the Salmonella typhi bacteria and spreads through contaminated food or water. It causes a sustained high fever and gastrointestinal symptoms like diarrhea and abdominal pain.
2. Diagnosis involves identifying the bacteria from blood or stool cultures. Treatment consists of antibiotics like chloramphenicol or ampicillin administered over 2-4 weeks.
3. Preventing transmission requires proper sanitation and hygiene practices like handwashing and boiling drinking water in areas where typhoid is common.
Lassa fever aka Lassa hemorrhagic fever is caused by lassa virus and is a Zoonotic disease. It is epidemic in Nigeria, Sierra Leone and Liberia.
Limiting direct contact between humans and rodents can help prevent this disease.
In this video, you can learn about the basics of Typhoid fever and also the symptoms and treatment of this disease in a very simple way. We describe to you here all about,
1. Typhoid fever
2. Symptoms of Typhoid
3. Causes of Typhoid
4. Diagnosis of Typhoid
5. Prevention of Typhoid
6. Treatment of Typhoid
7. Diet for Typhoid fever
You can download the PowerPoint file from below link:
https://docs.google.com/presentation/d/1s8Ix3t8t3O-KYWVze2C8nm4QYIWJdFSXg_sTR78htiQ/edit?usp=sharing
You can learn from video by the below link:
https://youtu.be/PDhr_UmTWuc
Bacteria of the genus Salmonella are highly adapted for growth in both humans and animals and cause a wide spectrum of disease.
The growth of S. Typhi and S. Paratyphi is restricted to human hosts, in whom these organisms cause enteric (typhoid) fever.
The remaining serotypes (non-typhoidal Salmonella or NTS) can colonize the gastrointestinal tracts of a broad range of animals, including mammals, reptiles, birds and insects.
Now a days.All the World is facing a serious problem..Dengue
so i make a presentation on dengue to prevent and aware from dengue...and if you have dengue faver then which types of treatment you use for your Health.
Lassa fever aka Lassa hemorrhagic fever is caused by lassa virus and is a Zoonotic disease. It is epidemic in Nigeria, Sierra Leone and Liberia.
Limiting direct contact between humans and rodents can help prevent this disease.
In this video, you can learn about the basics of Typhoid fever and also the symptoms and treatment of this disease in a very simple way. We describe to you here all about,
1. Typhoid fever
2. Symptoms of Typhoid
3. Causes of Typhoid
4. Diagnosis of Typhoid
5. Prevention of Typhoid
6. Treatment of Typhoid
7. Diet for Typhoid fever
You can download the PowerPoint file from below link:
https://docs.google.com/presentation/d/1s8Ix3t8t3O-KYWVze2C8nm4QYIWJdFSXg_sTR78htiQ/edit?usp=sharing
You can learn from video by the below link:
https://youtu.be/PDhr_UmTWuc
Bacteria of the genus Salmonella are highly adapted for growth in both humans and animals and cause a wide spectrum of disease.
The growth of S. Typhi and S. Paratyphi is restricted to human hosts, in whom these organisms cause enteric (typhoid) fever.
The remaining serotypes (non-typhoidal Salmonella or NTS) can colonize the gastrointestinal tracts of a broad range of animals, including mammals, reptiles, birds and insects.
Now a days.All the World is facing a serious problem..Dengue
so i make a presentation on dengue to prevent and aware from dengue...and if you have dengue faver then which types of treatment you use for your Health.
Typhoid fever, also known as enteric fever, is a potentially fatal multisystemic illness caused primarily by Salmonella enterica, subspecies enterica serovar typhi and, to a lesser extent, related serovars paratyphi A, B, and C.
The protean manifestations of typhoid fever make this disease a true diagnostic challenge. The classic presentation includes fever, malaise, diffuse abdominal pain, and constipation. Untreated, typhoid fever is a grueling illness that may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death within 1 month of onset. Survivors may be left with long-term or permanent neuropsychiatric complications.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
2. Aetiology
• Typhoid fever is caused by Enterobacteriaceae, genus
Salmonella.
• The microorganism is motile. Pathogenic only towards
human.
• It is stable in the environment:
in running water it persists for 5-10 days
in stagnant water for a few months.
It can survive over winter in ice.
3. Aetiology
In fruits and vegetables it lives for 5-10 days
In other foods from 2 to 8 weeks.
On some objects of the environment it persists from several
hours to a month and even longer.
• When dried in direct sun light the pathogenic microorganism is
rapidly destroyed.
• A 3 % solution of lysol and a 3 % chloramine solution kill the
bacteria within 2-3 minutes and Boiling kills it instantaneously.
4. Epidemiology
•The source of infection is a typhoid patient or a
carrier.
•Patients with typhoid fever are contagious for the
surrounding people beginning with the 1st week of the
disease.
•They are the greatest danger during the 2nd and 3rd
week of the disease as the maximum amount of
pathogenic microorganisms are excreted in the urine
and stools.
5. Epidemiology
• Beginning with the first week of the disease, specific immunity
develops in most patients. This helps the patient to free from
the pathogenic microorganisms and to terminate toxaemia.
• The leading role in the spread of infection belongs to chronic
carriers, especially if they are engaged occupationally in
handling of food that is not cooked before use.
• Chronic carriers are dangerous not only as the source of
infection, but also as depots of typhoid infection.
6. The Mechanism of Transmission
• Typhoid fever is characterized by the faecal-oral mechanism of
infection.
• The pathogenic microorganisms are released from the patient or carrier
with faeces and urine, and enter the body of a healthy person with
water or food.
• The transmission factors are:
Water
Food
Soiled hands
Environmental objects such as dishes, toys, linen, towels, flies,etc…
7. The Mechanism of Transmission
• If infection is transmitted with water, the morbidity rate depends on a
particular source of water: water supply system, river, well, pond.
• Water-borne epidemics of typhoid fever can be classed as:
1. Acute, that develop periodically and last over a comparatively short
period of time;
2. Chronic, that last for a few months and even years.
8. The Mechanism of Transmission
• Acute water-borne epidemics result from breakdown in the
water supply system or neglected rules of their maintenance.
• Chronic water-borne epidemics develop as a result of
systematic contamination of water with surface pollutants
through maintenance wells or some other routes.
• Food-borne transmission is characterized by ingestion of
contaminated milk and dairy products, and dishes not cooked
before consumption.
9. The Mechanism of Transmission
•During transmission of infection by person-to-person
contact, the microorganism is transmitted from the
patient or a carrier to a healthy person directly through
soiled hands or infected environmental objects. Spread
of infection is facilitated by suboptimal sanitation and
poor socio-economic conditions.
•If sanitation is inadequate and disposal of wastes is
below standards, flies promote the spread of typhoid
fever.
10. The Mechanism of Transmission
•Typhoid fever occurs in various countries but the
incidence is never pandemic, because typhoid fever is
characterized by a prolonged incubation period and the
maximum amount of pathogenic microorganisms are
released by the patient in 2-3 weeks after the onset of
the disease, that is, when the patient is already
hospitalized.
•The incidence is the highest during the warm season
(summer and autumn).
11. Pathogenesis
• The pathogenic microorganisms enter a human through the
mouth.
• If the defensive function of the stomach is adequate, the
microorganism is killed in the stomach and the person does not
develop the disease.
• If the defense function is impaired and the number of
microorganisms that enter the stomach is great, they can reach
the lower portions of the small intestine where they get into the
aggregations of lymphatic follicles (Peyer's plaques) and
solitary follicles, and into the nearest mesenteric lymph nodes,
where they multiply.
12. Pathogenesis
• At the end of the incubation period ,the pathogenic microorganisms
are released from the mesenteric nodes into the blood to cause
bacteraemia. The pathogenic microorganisms are thus carried
throughout the entire body and precipitate in the spleen, bone
marrow, lymph nodes and the liver.
• As the microbes die, they release endotoxin that poisons the body.
The endotoxin acts on the central nervous system to induce status
typhosus, which is characterized by dimmed consciousness,
inhibition, sleepiness alternated by insomnia, headache.
13. Pathogenesis
• The rate of bacteria removal from the patient depends largely
on the function of the excretory organs and systems (the liver,
the intestinal glands, the intestine, the kidneys) and formation of
specific antibodies.
14. Pathogenesis
• From the liver, the microbes are released with bile into the intestine and
are partly excreted from the patient. The remaining microbes precipitate
in aggregated and single lymphatic follicles in the lower portion of the
small intestine. The re-entrance of the microbes into the presensitized
aggregated and solitary lymphatic follicles causes an allergic
inflammation with ulceration and necrosis of tissues.
• Involvement of the sympathetic nervous system induces meteorism
(inflation of the intestine), diarrhoea, bradycardia, and hypotension.
• Endotoxin affects also bone marrow and induces leucopenia.
15. Clinical picture
• The incubation period lasts from 7 to 25 days (usually 14 days).
• The disease begins with a prodromal period. The patient
gradually develops:
• Weakness
• Malaise
• Chills
• Headache
• Impaired Appetite
16. Clinical picture
• The period lasts from a few hours to 2 days. The symptoms
then gradually intensify. The subjective condition impairs. The
patient develops
• Lack of Strength,
• Lack of Interest,
• Headache,
• Suffers from insomnia.
• Weakness makes the patient keep his bed.
17. Clinical picture
•The body temperature rises in steps, and by the 4th or
5th day it is 39-40 °C. For a period of time it remains
constantly high and then undulant fever develops.
•In the absence of specific treatment high fever can
persist for 2-3 weeks and then body temperature
decreases to normal in 4-5 weeks.
19. Clinical picture
• Visible mucosa and Skin pallor
• The tongue is thick, with imprints of the teeth by its edge; the tongue is
white, while the margins and the tip are free from the coat and are
crimson. If the disease runs a severe course, the tongue becomes dry,
its surface is cracked, the coat is stained with blood and turns brownish.
• The abdomen is inflated due to accumulation of a great amount of gas.
Constipation develops (diarrhoea is less common). The spleen becomes
enlarged by the end of the 1st week; the liver is enlarged later. The
pulse rate does not agree with the body temperature (relative
bradycardia); arterial pressure falls.
20. Clinical picture
• Rose spots occur on the abdomen, less frequently on the chest in 8-9
days of illness. The rash persists for 4-5 days and then regresses. Fresh
spots develop on new sites of the skin. In severe cases the rash can
bleed.
21. Clinical picture
• At the height of the disease, beginning with the 5th or 7th day, as
the fever intensifies, the nervous system is involved and the
status typhosus develops. The patient becomes indifferent,
delirium develops, headache intensifies along with increasing
meteorism and insomnia. In severe cases stupor develops
which can transform into sopor.
• A transient moderate leucocytosis is followed by leucopenia
with a relative lymphocytosis (40-60 %), aneosinophilia and
thrombocytopenia; ESR is moderately accelerated.
22. Clinical picture
• Bronchopneumonia and pharyngitis ulcerosa can develop at the
height of the disease; protein and casts can be found in the urine.
• Oliguria develops.
• Bacteriuria is associated with lesions of the urinary tract (pyelitis,
cystitis).
• As the clinical manifestations abate, toxaemia lessens, body
temperature gradually drops, sleep is normalized, appetite improved, the
tongue clears of the coat, and the amount of urine excreted increases.
After normalization of body temperature, the patient begins recovering.
23. Diagnosis
• The diagnosis of typhoid fever is based on the:
• Clinical picture of the disease
• Epidemiologic anamnesis
• Laboratory findings.
• The main method of laboratory diagnosis is bacteriologic study.
• The blood
• Urine
• Faeces
• Bile (duodenal contents) are examined in the laboratory.
24. Diagnosis
• The blood culture method is rapid and accurate for early diagnosis.
Blood cultures are mostly positive during the first days of the disease,
before antibiotic therapy is started.
• The immunofluorescence method is also used for early diagnosis of
typhoid fever. It reveals the typhoid bacillus in 10-12 hours after
inoculation.
• Stool and urine cultures are less important because they are positive
only beginning with the second week of the disease. Cultures are
inoculated from the first day of the disease.
25. Diagnosis
• In order to reveal carriers, the duodenal contents should be :
• Examined not earlier than 5-10 days following the fall of
temperature. Bile is taken from a fasting patient using a
duodenal tube.
• Serologic studies are used to confirm the diagnosis.
• In order to differentiate acute carriers from chronic ones, and
also vaccinated persons from carriers, indirect
haemagglutination tests with cysteine are used.
26. Treatment
• Chloramphenicol is used to treat typhoid fever. It is given in doses from 0.5 to 0.75 g four times
a day until the body temperature normalizes, and then for another 8-10 days (0.5 g three times a
day). Chloramphenicol is given per os, 20-30 minutes before meals. If vomiting develops,
chloramphenicol sodium succinate should be given intramuscularly or intravenously, 1.0 g three
times a day.
• Ampicillin in doses of 1 g four times a day (for 14 days) is also effective.
• Bactrim (biseptol), 2-3 tablets two times a day (for 3-4 weeks), or nitrofurane preparations in
doses of 0.15-0.2 g four times a day are given to patients with antibiotic-resistant bacilli.
• Antibiotics combined with vaccines decrease the incidence of relapses and prevent carrier state.
• An immediate surgical operation is necessary in intestinal perforation.