Tuesday 8 August 2023

Dengue Fever : What should you know ?

Dengue: Symptoms, Prevention, and Treatment**

**Author: Dr. Koushik Debnath, MD (Clinical Microbiology and Infectious Diseases)**

Dengue fever is a viral illness that continues to be a major global health concern, particularly in tropical and subtropical regions. As a specialist in Clinical Microbiology and Infectious Diseases, I find it crucial to shed light on this disease, its symptoms, preventive measures, and available treatments. In this article, we will delve into the nuances of dengue and provide essential information for both the general public and medical professionals.

**Introduction to Dengue:**

Dengue is caused by the dengue virus, which is primarily transmitted to humans through the bites of infected Aedes mosquitoes, particularly Aedes aegypti and Aedes albopictus. This virus is classified into four serotypes, labeled as DEN-1, DEN-2, DEN-3, and DEN-4. Once infected, individuals can develop mild to severe symptoms.

**Symptoms and Clinical Presentation:**

Common symptoms of dengue include high fever, severe headache, joint and muscle pain, skin rash, and mild bleeding. In severe cases, dengue can progress to dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS), which can lead to bleeding, organ impairment, and even death if not promptly managed.

**Preventive Measures:**

1. **Mosquito Control:** The primary method of preventing dengue is to control mosquito populations. This can be achieved by eliminating standing water where mosquitoes breed, using mosquito nets, and applying insect repellents.

2. **Personal Protection:** Wearing long-sleeved clothing and using mosquito repellents when outdoors can significantly reduce the risk of mosquito bites.

3. **Community Efforts:** Community engagement in maintaining clean surroundings and preventing water accumulation is crucial in minimizing mosquito breeding sites.

**Diagnosis and Treatment:**

Diagnosing dengue involves clinical evaluation, combined with laboratory tests like serological tests and molecular assays. Early detection is essential to prevent severe complications. Unfortunately, there is no specific antiviral treatment for dengue. Management primarily involves supportive care, including hydration, fever-reducing medications, and monitoring for complications.

**Future Directions:**

Efforts to combat dengue include ongoing research into vaccine development. The first dengue vaccine, Dengvaxia, has been approved for limited use in certain regions, but its efficacy and safety have been subjects of debate. Further research is needed to develop effective vaccines that protect against all serotypes.


Dengue remains a significant public health challenge, particularly in regions where Aedes mosquitoes thrive. Education, mosquito control, and community engagement play pivotal roles in preventing and managing dengue outbreaks. As a specialist in Clinical Microbiology and Infectious Diseases, my aim is to create awareness about this disease and emphasize the importance of collaborative efforts in its prevention and control.

Remember, staying informed and taking proactive measures can greatly contribute to reducing the impact of dengue on individuals and communities.

Tuesday 6 June 2023

Diabetic Nephropathy: Diagnosis, Management, and Treatment for Optimal Kidney Health

      Diabetic nephropathy is a chronic kidney disease that is one of the most common complications of diabetes mellitus. It is characterized by the gradual deterioration of kidney function, leading to proteinuria, hypertension, and eventually end-stage renal disease (ESRD). Early detection, accurate diagnosis, and proper management of diabetic nephropathy are crucial to slow down disease progression and improve patient outcomes. This article aims to provide a comprehensive guide to the diagnosis and management of diabetic nephropathy.


1. Screening and Early Detection:

   - Regular screening of individuals with diabetes is essential to detect the onset of kidney damage at an early stage.

   - Urine albumin excretion rate (AER) and albumin-to-creatinine ratio (ACR) are used to assess albuminuria.

   - Estimated glomerular filtration rate (eGFR) is calculated using equations such as the Modification of Diet in Renal Disease (MDRD) or Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula.

   - Screening should begin at the time of diabetes diagnosis for type 2 diabetes and within 5 years of diagnosis for type 1 diabetes.

2. Staging and Diagnosis:

   - Diabetic nephropathy is staged based on albuminuria and eGFR as per the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines.

   - Stages include normoalbuminuria, microalbuminuria, macroalbuminuria, and ESRD.

   - Additional tests, such as renal ultrasound and kidney biopsy, may be conducted to evaluate kidney structure and determine the underlying cause.


1. Glycemic Control:

   - Intensive glycemic control through lifestyle modifications, oral hypoglycemic agents, or insulin therapy can significantly delay the onset and progression of diabetic nephropathy.

   - HbA1c levels should be maintained below the recommended targets, considering individual patient characteristics and comorbidities.

2. Blood Pressure Management:

   - Optimal blood pressure control is vital to slow the progression of kidney disease.

   - The target blood pressure goal for most patients with diabetic nephropathy is <130/80 mmHg.

   - Lifestyle modifications and antihypertensive medications, including ACE inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs), are commonly prescribed.

3. Proteinuria Management:

   - Reducing proteinuria is an essential therapeutic goal.

   - ACEIs and ARBs not only control blood pressure but also reduce proteinuria.

   - Other agents, such as direct renin inhibitors and aldosterone antagonists, may be considered in resistant cases.

4. Dyslipidemia Management:

   - Dyslipidemia is commonly associated with diabetic nephropathy and increases the risk of cardiovascular disease.

   - Statins and fibrates are frequently prescribed to manage dyslipidemia and reduce cardiovascular risk.

5. Sodium and Fluid Restriction:

   - Dietary sodium restriction is recommended to manage hypertension and fluid retention.

   - Fluid intake should be adjusted based on individual patient needs and urine output.

6. Smoking Cessation and Lifestyle Modifications:

   - Encouraging smoking cessation and adopting a healthy lifestyle, including regular exercise, weight management, and a balanced diet, are essential components of diabetic nephropathy management.

7. Monitoring and Follow-up:

   - Regular monitoring of kidney function, blood pressure, glycemic control, and proteinuria is necessary to evaluate the response to treatment and identify any progression of the disease.

   - Patient education and adherence to treatment regimens play a crucial role in achieving optimal outcomes.

Saturday 3 June 2023

Unleashing the Potential of Probiotics: Cultivating Gut Health for Optimal Well-being


        Probiotics have emerged as a groundbreaking solution for enhancing gut health and promoting overall well-being. In this article, we will delve into the tremendous potential of probiotics, highlighting their role in nurturing a healthy gut and optimizing our overall physical and mental health. Discover how incorporating probiotics into your daily routine can contribute to a happier and healthier lifestyle.

Section 1: Understanding the Power of Probiotics

     Probiotics are live bacteria and yeasts that offer numerous health benefits when consumed in adequate amounts. These beneficial microorganisms play a vital role in maintaining a balanced gut environment, aiding digestion, and supporting immune function.

Section 2: Nurturing Gut Health with Probiotics

     By incorporating probiotics into your daily routine, you can create a thriving environment in your gut. Probiotics work by replenishing and restoring the natural balance of beneficial bacteria, which may be disrupted by factors such as poor diet, stress, or antibiotic use. By nurturing your gut health, you lay the foundation for overall well-being.

Section 3: Optimizing Physical Health with Probiotics

      Probiotics have been shown to improve various aspects of physical health. They enhance nutrient absorption, aid in weight management, and contribute to a healthy cardiovascular system. Additionally, probiotics can alleviate symptoms associated with gastrointestinal disorders such as irritable bowel syndrome (IBS) and promote regular bowel movements.

Section 4: Boosting Mental Health and Well-being

      The gut and brain are intricately connected through the gut-brain axis. Probiotics have been found to influence mental health by modulating the production of neurotransmitters, reducing stress levels, and improving mood. Incorporating probiotics into your diet can be a proactive step towards maintaining a healthy mind and emotional balance.

Section 5: Embracing a Healthier Lifestyle

     By harnessing the power of probiotics, you can embrace a healthier lifestyle. Incorporate probiotic-rich foods such as yogurt, sauerkraut, and kefir into your diet. Alternatively, opt for high-quality probiotic supplements to ensure an adequate intake. Combined with regular exercise and a balanced diet, probiotics can contribute to a holistic approach to well-being.


     Probiotics offer a multitude of benefits for nurturing gut health and promoting overall well-being. By understanding the power of probiotics and incorporating them into your daily routine, you can optimize your physical and mental health, paving the way for a happier and healthier lifestyle. Take the proactive step towards harnessing the potential of probiotics and experience the transformative impact they can have on your overall well-being.

Thursday 1 June 2023

"Unveiling the Hidden Dangers: Exploring the Health Risks of Secondhand Smoking"

Secondhand smoking, also known as passive smoking or involuntary smoking, is a serious concern that affects both smokers and non-smokers alike. This article aims to shed light on the risks associated with secondhand smoking and its impact on our overall lifestyle and well-being. By increasing our awareness of these dangers, we can make informed decisions to protect ourselves and those around us from the harmful effects of secondhand smoke.

1. The Concept of Secondhand Smoking:
Secondhand smoking refers to the inhalation of tobacco smoke by individuals who are not actively smoking themselves. This can occur in various settings, such as homes, workplaces, public spaces, or even in vehicles. The smoke released from burning cigarettes, cigars, or pipes contains more than 7,000 chemicals, including at least 70 known to cause cancer.

2. Health Risks Associated with Secondhand Smoking:
Exposure to secondhand smoke poses numerous health risks, making it a major public health concern. These risks include:

a) Increased Risk of Cancer:
Secondhand smoke contains carcinogens, substances that can lead to the development of cancer. Non-smokers who are regularly exposed to secondhand smoke have a higher risk of developing lung cancer, as well as other forms of cancer, such as breast, bladder, and throat cancer.

b) Respiratory Issues:
Inhaling secondhand smoke can have immediate and long-term effects on the respiratory system. It can cause or exacerbate conditions such as asthma, bronchitis, and pneumonia. Children exposed to secondhand smoke are particularly susceptible to developing respiratory infections and experiencing more severe symptoms.

c) Cardiovascular Complications:
Secondhand smoke can have detrimental effects on the cardiovascular system. It increases the risk of heart disease, stroke, and other cardiovascular conditions in both adults and children. Non-smokers exposed to secondhand smoke may experience elevated blood pressure, reduced lung function, and an increased risk of blood clots.

d) Impact on Children:
Children are especially vulnerable to the hazards of secondhand smoking. Exposure to secondhand smoke during infancy and childhood increases the risk of sudden infant death syndrome (SIDS), respiratory infections, asthma, ear infections, and impaired lung development.

3. Protecting Yourself and Others:
To minimize the risks associated with secondhand smoke, it is crucial to take proactive measures:

a) Create Smoke-Free Environments:
Encourage smoke-free policies in your home, car, and workplace. Establishing designated smoking areas away from non-smokers can help reduce exposure.

b) Support Smoking Cessation:
If you or someone close to you is a smoker, consider seeking support to quit smoking. Quitting not only benefits your own health but also protects those around you from secondhand smoke.

c) Advocate for Smoke-Free Public Spaces:
Support initiatives that promote smoke-free environments in public spaces, such as parks, restaurants, and recreational areas. Encourage policymakers to implement and enforce smoking bans to safeguard the health of the community.

d) Education and Awareness:
Spread knowledge about the risks of secondhand smoke. Educate friends, family, and colleagues about the importance of avoiding exposure to secondhand smoke and its detrimental effects on health.

Secondhand smoking poses significant risks to our health and well-being, affecting both smokers and non-smokers. By understanding the dangers associated with secondhand smoke and taking proactive steps to protect ourselves and others, we can create a healthier and smoke-free environment. Prioritizing smoke-free spaces and supporting smoking cessation efforts will contribute to a better quality of life for everyone.

Unveiling HMPV: A Comprehensive Guide to the Spreading Virus in the US


HMPV, short for Human Metapneumovirus, is a virus that is currently spreading in the United States. It's important to understand what this virus is and how it can affect us. In this article, we will provide you with an easy-to-understand explanation of HMPV and its key characteristics.

1. What is HMPV?

HMPV is a type of virus that primarily affects the respiratory system. It belongs to the same family as the common cold and respiratory syncytial virus (RSV). It was first identified in 2001 and has since been recognized as a common cause of respiratory infections, especially in young children and older adults.

2. How does HMPV spread?

HMPV spreads from person to person through respiratory droplets when an infected individual coughs or sneezes. These droplets can then be inhaled by nearby individuals, leading to infection. It can also spread by touching surfaces contaminated with the virus and then touching the face.

3. What are the symptoms?

The symptoms of HMPV are similar to those of other respiratory infections. They may include cough, runny nose, sore throat, fever, and difficulty breathing. In severe cases, it can lead to pneumonia or bronchiolitis, particularly in young children or individuals with weakened immune systems.

4. Who is at risk?

While HMPV can affect people of all ages, it is more likely to cause severe illness in infants, young children, older adults, and individuals with underlying health conditions. These individuals should take extra precautions to avoid exposure to the virus.

5. How can HMPV be prevented?

Preventing the spread of HMPV involves practicing good hygiene and taking precautions to minimize exposure. Some preventive measures include:

- Washing hands frequently with soap and water for at least 20 seconds.

- Using hand sanitizers if soap and water are not readily available.

- Covering the mouth and nose with a tissue or elbow when coughing or sneezing.

- Avoiding close contact with individuals showing symptoms of respiratory infection.

- Disinfecting frequently-touched surfaces regularly.

6. Is there a specific treatment ?

Rest with supportive care, such as getting plenty of rest, staying hydrated, and using over-the-counter medications to alleviate symptoms. In severe cases, hospitalization may be required.

7. When should I seek medical attention?

If you or a loved one experience severe symptoms, such as persistent high fever, difficulty breathing, or worsening cough, it is advisable to seek medical attention promptly. Healthcare professionals can provide a proper diagnosis and offer appropriate treatment recommendations.


HMPV is a respiratory virus that is spreading in the United States. It can cause symptoms similar to the common cold or more severe respiratory infections. By practicing good hygiene, taking preventive measures, and seeking medical attention when necessary, we can minimize the spread and impact of HMPV. Stay informed and take care of your health and well-being.

Rheumatoid Arthritis: A Comprehensive Overview of Pathogenesis, Clinical Features, Diagnosis, and Treatment

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent inflammation of the synovial joints. It affects approximately 1% of the global population and can lead to significant disability if left untreated. This article provides a detailed review of the pathogenesis, clinical features, diagnosis, and treatment options for rheumatoid arthritis.

1. Introduction:

Rheumatoid arthritis is a systemic autoimmune disorder primarily affecting the joints. It is characterized by chronic inflammation of the synovial membranes, leading to progressive destruction of articular cartilage and bone. The disease often leads to joint deformity, functional impairment, and a reduced quality of life for affected individuals.

2. Pathogenesis:

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammation of the joints. It primarily affects the synovial lining of the joints, leading to pain, swelling, stiffness, and eventually joint deformity and functional impairment. The pathogenesis of rheumatoid arthritis is complex and involves multiple genetic, environmental, and immunological factors.

*Genetic Factors:

There is evidence to suggest a genetic predisposition to rheumatoid arthritis. Certain genes, such as the human leukocyte antigen (HLA) genes, specifically the HLA-DRB1 allele, are strongly associated with an increased risk of developing RA. However, having these genetic markers does not guarantee the development of the disease, indicating that other factors play a role as well.

*Environmental Factors:

Various environmental factors have been implicated in the development of rheumatoid arthritis. These include smoking, which is the most significant environmental risk factor for RA. Exposure to certain infections, such as Epstein-Barr virus and Porphyromonas gingivalis, a bacterium involved in gum disease, has also been associated with an increased risk of developing RA.

*Immune System Dysfunction:

The immune system plays a critical role in the pathogenesis of rheumatoid arthritis. In individuals susceptible to the disease, an initial trigger, such as an infection or environmental factor, activates the immune system inappropriately. This leads to a cascade of events involving both innate and adaptive immune responses.

*Inflammatory Response:

The activated immune cells release pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6). These cytokines promote inflammation and recruit additional immune cells to the joints, causing synovial tissue inflammation and subsequent destruction of cartilage and bone.

*Autoantibody Production:

In rheumatoid arthritis, the immune system produces autoantibodies, specifically rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies. These autoantibodies target self-proteins, such as immunoglobulins and citrullinated peptides, forming immune complexes that contribute to the inflammatory response and joint damage.

*Synovial Hyperplasia:

The chronic inflammation in the synovial lining of the joints leads to synovial hyperplasia, characterized by increased cell proliferation and infiltration of immune cells. The hyperplastic synovium, known as pannus, invades the adjacent cartilage and bone, causing erosion and destruction.

*Osteoclast Activation:

   Activated immune cells and inflammatory cytokines stimulate the production and activation of osteoclasts, cells responsible for bone resorption. Osteoclast activation leads to the destruction of the underlying bone in affected joints, further contributing to joint deformities and functional impairment.

Overall, the pathogenesis of rheumatoid arthritis involves a complex interplay of genetic, environmental, and immunological factors. While the exact trigger and mechanisms underlying the disease are not yet fully understood, ongoing research aims to shed light on the pathogenic pathways involved. Understanding the pathogenesis of RA is crucial for the development of targeted therapies and interventions to better manage this chronic autoimmune condition.

3. Clinical Features:

The clinical presentation of rheumatoid arthritis varies among individuals, but commonly includes joint pain, swelling, stiffness, and functional limitations. Typically, RA affects the small joints of the hands and feet symmetrically. Systemic symptoms such as fatigue, malaise, and low-grade fever may also be present. Extra-articular manifestations can involve other organs, such as the skin, eyes, lungs, and heart.

4. Diagnosis:

Diagnosing rheumatoid arthritis requires a combination of clinical assessment, laboratory tests, and imaging studies. Key diagnostic criteria include the presence of symmetric joint swelling and morning stiffness lasting for at least one hour. Blood tests for rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies are helpful in confirming the diagnosis. Imaging modalities like X-rays and ultrasound can detect joint erosions and synovitis.

5. Treatment:

The management of rheumatoid arthritis aims to control disease activity, relieve symptoms, and prevent joint damage. Treatment strategies often involve a multidisciplinary approach, including pharmacological interventions, physical therapy, and patient education. Nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids provide symptomatic relief, while disease-modifying anti-rheumatic drugs (DMARDs) such as methotrexate and biologic agents target the underlying immune response. Early intervention and aggressive treatment have been shown to improve outcomes and slow disease progression.

6. Future Perspectives:

Ongoing research in rheumatoid arthritis focuses on identifying novel therapeutic targets and developing personalized treatment strategies. Advances in biologic agents, targeted synthetic DMARDs, and regenerative medicine hold promise for improved disease control and long-term outcomes. Additionally, lifestyle modifications, such as regular exercise and smoking cessation, can play a crucial role in the management of RA.


Rheumatoid arthritis is a chronic autoimmune disorder characterized by joint inflammation and destruction. Early diagnosis and aggressive treatment are essential for optimal outcomes. A comprehensive understanding of the pathogenesis, clinical features, diagnostic approaches, and treatment options can guide healthcare professionals in effectively managing this complex disease and improving the quality of life for patients with rheumatoid arthritis.

Wednesday 31 May 2023

Real-Time PCR: Unveiling the Importance of CT Value in Infectious Disease Treatment



      Infectious diseases continue to pose a significant threat to public health globally. The ability to rapidly and accurately diagnose these diseases is crucial for effective treatment and containment. Real-time polymerase chain reaction (PCR) has revolutionized the field of infectious disease diagnostics, allowing for precise and timely detection of pathogens. One of the key parameters derived from real-time PCR analysis is the CT value, which holds immense importance in guiding treatment decisions and monitoring disease progression. This article aims to explore the concept of real-time PCR and delve into the significance of the CT value in the context of infectious disease treatment.

Understanding Real-Time PCR:

       Polymerase chain reaction (PCR) is a laboratory technique used to amplify a specific segment of DNA or RNA from a complex mixture. Traditional PCR involves multiple cycles of amplification and requires a separate step for detecting the amplified product post-amplification. Real-time PCR, also known as quantitative PCR (qPCR), is an advanced version that allows the detection of amplified DNA or RNA in real-time as the reaction progresses. This real-time monitoring is achieved by incorporating fluorescent dyes or probes into the reaction mixture.

     Real-time PCR is a highly sensitive and specific technique that enables the rapid identification and quantification of nucleic acids. It is widely employed for diagnosing various infectious diseases, including viral, bacterial, and fungal infections. By targeting specific regions of the pathogen's genetic material, real-time PCR can confirm the presence of the infectious agent with high accuracy.

The Significance of the CT Value:

      The CT value, also referred to as the cycle threshold or quantification cycle (Cq), is a crucial parameter derived from real-time PCR analysis. It represents the cycle number at which the fluorescence signal generated by the amplification reaches a specific threshold level. The CT value is inversely proportional to the amount of target nucleic acid initially present in the sample. A lower CT value indicates a higher initial target concentration, while a higher CT value suggests a lower initial target concentration.

      In the context of infectious disease treatment, the CT value holds significant importance for several reasons:

1. Diagnostic Potential: 

      The CT value provides a quantitative measure of the pathogen's load in a clinical sample. By comparing the CT value obtained from a patient's sample to established reference ranges, clinicians can determine whether an infection is present, aiding in accurate diagnosis.

2. Monitoring Disease Progression:

      During the course of an infection, the CT value can serve as an indicator of disease progression or response to treatment. A decreasing CT value over time suggests a reduction in pathogen load, indicating successful treatment. Conversely, an increasing CT value may indicate treatment failure or the emergence of drug resistance.

3. Treatment Guidance: 

      The CT value can help guide treatment decisions, particularly in the case of viral infections. Different viral infections have varying levels of virulence and response to antiviral medications. By monitoring the CT value over time, clinicians can assess the effectiveness of antiviral therapy and make adjustments accordingly.

4. Contagiousness Assessment

         The CT value can provide insights into the contagiousness of an individual infected with a particular pathogen. Lower CT values indicate higher viral loads and suggest that the patient may be more contagious. This information can assist in implementing appropriate infection control measures to limit the spread of the disease.

5. Prognostic Indicator:

       In some cases, the CT value has been correlated with the severity of the disease and patient outcomes. Studies have shown that a higher CT value at the time of diagnosis may be associated with a milder course of illness, while a lower CT value may indicate a higher risk of complications or adverse outcomes.


      Real-time PCR has revolutionized infectious disease diagnostics, providing rapid and accurate detection of pathogens.

Saturday 27 May 2023

What is Blood Culture in ID Diagnostics ?

As a medical professional, it's important to understand the role of blood culture in diagnosing and treating various infections. Blood culture is a diagnostic test that involves collecting a sample of blood from a patient and culturing it to identify the presence of bacteria or other microorganisms that may be causing an infection. In this blog, we will discuss the importance of blood culture, how it is performed, and what factors can affect its accuracy.

Why is Blood Culture Important?

Blood culture is an important diagnostic tool in the field of medicine as it helps in identifying the causative agent of an infection. It is particularly useful in cases where the source of infection is unknown, or where the clinical symptoms are not specific enough to suggest a particular type of infection. Blood culture can also help in identifying the extent of the infection and determining the appropriate course of treatment.

How is Blood Culture Performed?

Blood culture is performed by collecting a sample of blood from a patient and culturing it in a laboratory. The sample is usually collected through a sterile needle that is inserted into a vein in the arm or hand. The collected blood is then placed into several culture bottles that contain a nutrient-rich growth medium. The culture bottles are then placed in an incubator where they are kept at a temperature that is optimal for the growth of microorganisms. The bottles are checked regularly for the growth of microorganisms, and if any are detected, they are identified and tested for antibiotic susceptibility.

Factors That Affect the Accuracy of Blood Culture-

Although blood culture is a highly accurate diagnostic test, there are several factors that can affect its accuracy. One of the most important factors is the timing of the sample collection. Blood culture should be performed as soon as possible after the onset of symptoms to increase the chances of detecting the causative agent. If the sample is collected too late, the microorganisms may no longer be present in the bloodstream, making it difficult to identify the infection.

Another important factor that can affect the accuracy of blood culture is the collection technique. The sample should be collected using a sterile needle and syringe to prevent contamination with bacteria from the skin. The skin should also be cleaned thoroughly with an antiseptic solution before the sample is collected.

Finally, the accuracy of blood culture can be affected by the type of microorganism that is causing the infection. Some microorganisms are more difficult to culture than others, and may require special growth media or longer incubation times to be detected.


Blood culture is an important diagnostic tool in the field of medicine. It helps in identifying the causative agent of an infection and determining the appropriate course of treatment. While blood culture is a highly accurate test, several factors can affect its accuracy, including the timing of the sample collection, the collection technique, and the type of microorganism causing the infection. As a medical professional, it's important to understand these factors and take steps to minimize their impact on the accuracy of blood culture results.

Friday 26 May 2023

Understanding Enteric Fever: Causes, Symptoms, and Treatment


      Enteric fever, also known as typhoid fever, is a bacterial infection primarily caused by Salmonella enterica serotype Typhi (S. Typhi) and, less commonly, by Salmonella enterica serotype Paratyphi (S. Paratyphi). It is a significant public health concern, particularly in regions with poor sanitation and limited access to clean water. In this blog, we will explore the causes, symptoms, diagnosis, and treatment options for enteric fever.

1. Causes of Enteric Fever:

      Enteric fever is primarily caused by consuming food or water contaminated with the Salmonella bacteria. The bacteria can survive in fecal matter, and transmission occurs through the oral-fecal route. Common causes of enteric fever include:

a) Contaminated Water: Drinking water contaminated with the Salmonella bacteria, typically from poor sanitation or sewage systems, is a significant source of infection.

b) Contaminated Food: Consuming food prepared under unhygienic conditions or using contaminated water for washing can lead to the ingestion of Salmonella bacteria.

c) Carrier Individuals: Individuals who have recovered from enteric fever but continue to harbor the bacteria in their gallbladder can be carriers and spread the infection to others.

2. Symptoms of Enteric Fever:

    Enteric fever is characterized by a wide range of symptoms, which can vary in severity. Common symptoms include:

a) High Fever: Sustained high fever, often gradually increasing over a few days, is a hallmark of enteric fever.

b) Gastrointestinal Symptoms: Abdominal pain, diarrhea, or constipation are common gastrointestinal symptoms associated with enteric fever.

c) Headache and Body Aches: Intense headache, body aches, and general malaise are frequently experienced by individuals with enteric fever.

d) Weakness and Fatigue: Persistent weakness and fatigue are common, leading to a significant impact on daily activities.

e) Rose Spots: A distinctive rash of rose-colored spots may appear on the trunk or abdomen in some individuals.

3. Diagnosis of Enteric Fever:

       Prompt and accurate diagnosis is crucial for effective management of enteric fever. Common diagnostic methods include:

a) Blood Culture: Isolating the bacteria from a blood sample is the gold standard for diagnosing enteric fever. 

b) Stool Culture: Testing a stool sample can help identify carriers or individuals with milder symptoms.

c) Serological Tests: Antibody-based tests, such as the Widal test, may be used to detect specific antibodies against Salmonella.

4. Treatment of Enteric Fever:

Enteric fever requires medical intervention, and treatment typically involves the following:

a) Antibiotics: Antibiotics like fluoroquinolones or third-generation cephalosporins are commonly prescribed to kill the Salmonella bacteria. However, antibiotic resistance is a growing concern, and treatment choices may vary based on local resistance patterns.

b) Supportive Care: Adequate hydration, rest, and maintaining a balanced diet are essential for recovery. Over-the-counter pain relievers can help manage fever and body aches.

c) Prevention: Vaccination against S. Typhi is available and recommended in areas with a high incidence of enteric fever. Additionally, practicing good hygiene, including handwashing and consuming safe food and water, is crucial in preventing the spread of the disease.


     Enteric fever, caused by Salmonella bacteria, is a significant health issue in many parts of the world. Early diagnosis and appropriate treatment with antibiotics are essential for a successful recovery. Additionally, preventive measures such as vaccination, maintaining good hygiene practices, and ensuring access to safe food and water play a vital role in reducing the incidence of enteric fever. If you experience symptoms suggestive of enteric fever, it is important to consult a healthcare professional for proper diagnosis and treatment.

Thursday 25 May 2023

Community acquired Pneumonia - What should you know ?


      Community-acquired pneumonia (CAP) is a common and potentially serious respiratory infection that affects individuals who have not been hospitalized or living in a long-term care facility within 14 days prior to the onset of symptoms. CAP can be caused by a variety of pathogens including bacteria, viruses, and fungi. In this article, we will discuss the epidemiology, etiology, pathophysiology, clinical features, diagnosis, and management of CAP.


       CAP is a significant cause of morbidity and mortality worldwide. It is estimated that approximately 4 million cases of CAP occur annually in the United States, resulting in over 1 million hospitalizations and 50,000 deaths. The incidence of CAP increases with age, with the highest rates observed among individuals over the age of 65. Other risk factors for CAP include chronic lung disease, heart disease, immunosuppression, and smoking.


                The etiology of CAP varies depending on the patient population, geographic location, and season. The most common bacterial pathogens responsible for CAP include Streptococcus pneumoniae, Haemophilus influenzae, and atypical bacteria such as Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella pneumophila. Viral pathogens such as influenza virus, respiratory syncytial virus, and adenovirus are also common causes of CAP, particularly in children. Fungal pathogens such as Pneumocystis jirovecii and Histoplasma capsulatum may cause CAP in immunocompromised individuals.


          CAP typically begins with the inhalation of a pathogen, which then colonizes the upper respiratory tract. If the host's immune defenses are compromised, the pathogen may spread to the lower respiratory tract and cause pneumonia. The pathophysiology of CAP involves an inflammatory response in the lungs, leading to alveolar damage, impaired gas exchange, and respiratory failure in severe cases.

Clinical Features-

     The clinical presentation of CAP can vary depending on the underlying pathogen, patient age, and comorbidities. Common symptoms include cough, fever, dyspnea, chest pain, and sputum production. Physical examination may reveal tachypnea, crackles on lung auscultation, and signs of respiratory distress. In severe cases, sepsis, shock, and acute respiratory distress syndrome (ARDS) may develop.


    The diagnosis of CAP is based on a combination of clinical features, laboratory tests, and imaging studies. Chest radiography is the most commonly used imaging modality to diagnose CAP, with typical findings including lobar or segmental consolidation, pleural effusions, and interstitial infiltrates.
    Blood cultures, sputum cultures, and respiratory viral panels may also be obtained to identify the underlying pathogen. In severe cases, arterial blood gas analysis and bronchoscopy with bronchoalveolar lavage may be necessary to confirm the diagnosis.


       The management of CAP depends on the severity of the illness and the underlying pathogen. Empirical antibiotic therapy should be initiated promptly for all patients with suspected CAP, with selection based on local resistance patterns and patient factors such as comorbidities and recent antibiotic use. Supportive care including oxygen therapy, bronchodilators, and fluid resuscitation should also be provided as needed. In severe cases, mechanical ventilation and vasopressor support may be necessary. Vaccination against S. pneumoniae and influenza have often proved helpful in decreasing the clinical severity of pneumonia in susceptible individuals. 

FAQs of CAP - 

a) What are the major causes of community acquired pnuemoniae ?  
   Streptococcus pneumoniae, Haemophilus influenzae,Moraxella catarrhalis, Chlamydia pneumoniae, Mycoplasma pneumoniae, Legionella species.

b) What is the most common treatment regimen of community acquired pneumoniae ? 
Depending on the local antibiotic policy, diagnostic parameters and patient's clinical condition 14 day regimen of Injection Ceftriaxone/Cefotaxime/Amoxicillin with or without addition of a macrolide like Azithromycin/Clarithromycin or Doxycline is considered as the treatment of choice. Iatroconazole can be considered if there is high degree suspicion of histoplasmosis or coccidioidomycosis. Treatment with Oseltamivir is considered for 5 days when respiratory secretions are Real Time RT-PCR positive for Influenza. 

      If you have any query feel free to drop us an email at consultation@drkoushikdebnath.com

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Wednesday 24 May 2023

Hypertension - A silent killer ?

Hypertension, also known as high blood pressure, is a common condition that affects millions of people worldwide. It occurs when the force of blood against the walls of the arteries is too high, which can lead to serious health problems such as heart disease and stroke. Fortunately, hypertension can be managed through a combination of lifestyle changes and medication.

Lifestyle Changes

The first step in managing hypertension is making lifestyle changes. These changes include:

1. Diet: Eating a healthy diet that is low in saturated and trans fats, salt, and added sugars can help manage hypertension. A diet rich in fruits, vegetables, whole grains, lean protein, and healthy fats such as olive oil can be beneficial. 

2. Exercise: Regular exercise can help lower blood pressure and improve overall health. It is recommended that adults engage in at least 150 minutes of moderate-intensity exercise per week, such as brisk walking, cycling, or swimming.

3. Weight management: Maintaining a healthy weight can help manage hypertension. Losing even a small amount of weight can make a big difference in blood pressure levels.

4. Stress management: Stress can increase blood pressure, so managing stress through techniques such as meditation, yoga, or deep breathing can be helpful.

5. Quit smoking: Smoking can increase blood pressure and damage the walls of the blood vessels. Quitting smoking can help manage hypertension and improve overall health.


In addition to lifestyle changes, medication may be necessary to manage hypertension. There are several types of medication that can be prescribed by a healthcare professional:

1. Diuretics: These medications help the body get rid of excess salt and water, which can lower blood pressure.

2. Angiotensin-converting enzyme (ACE) inhibitors: These medications block the production of a hormone that narrows blood vessels, which can lower blood pressure.

3. Calcium channel blockers: These medications relax blood vessels, which can lower blood pressure.

4. Beta-blockers: These medications slow the heart rate and reduce the force of the heart's contractions, which can lower blood pressure.

5. Renin inhibitors: These medications block the production of renin, a hormone that can narrow blood vessels and increase blood pressure.

It is important to work closely with a healthcare professional to determine the best medication and dosage for managing hypertension.


Hypertension is a common condition that can lead to serious health problems if left unmanaged. Fortunately, hypertension can be managed through a combination of lifestyle changes and medication. By making healthy lifestyle choices and working closely with a healthcare professional, people with hypertension can lower their blood pressure and reduce their risk of complications.

Health Tips for Summer and Monsoon - Must know points

     Summer is at peak in most of the Indian states now with temperature peaking at 40-45 deg celcius. On top of that, monsoon is also knocking at door which essentially means weather will be hot and humid over most of the eastern , sounthern, north eastern parts of the country over next few months. This particular climate condition is often suitable for transmission of different tropical infections like infectious gastroenteritis like Non Typhoidal Salmonellosis, Shigellosis, Malaria, Scrub Typhus along with upper respiratory infections of diverse etiology. 

How to maintain health in summer season ? 

- Wear loose fitting cotton garments preferably of light colour which have got lower rate of UV rays absorbtion.
- Keep yourself hydrated with plenty of water. Minimum water intake should be such that urine output remains at 0.5-1mL/kg/hr for a healthy adult individual.
Fluids with added sugar, preservatives, artificial falvouring substances, caffeine etc should be avoided. 
- Sunglasses, Skin Protective gloves, Sunscreen with SPF >30 should be used while going outdoor. 
- Less oily , Less spicy food should be on the preference list as these foods are easy on the stomach for digestion in these summer months. 

How is summer healthier than winter ?
    Winter is often cozy than summer months for most of the individuals. Winter is also the most favourite season for picnics, hangouts, tourism etc for most of us. Having said that, summer has its own advantages. Increased sun exposure boosts our Vitamin D levels , reduces oxidative stress and boosts our serotonin levels. On top of that there is relatively decreased risk for acute coronary syndrome, cerebrovascular incidents etc due to overall vasodilatated state with lesser sympathetic drive specially in vulnerable group of elderly patients. 

Treatment of Common ailments in Summer -

     Before you visit Doctor for treatment, do not forget to follow some basic practices. If you are suffering from loose motion take plenty of ORS( 1 full sachet in 1 L water) and for febrile spells take Paracetamol Tablets 650 twice daily. Beyond that never self medicate or buy over the counter medicines. Do consult your Doctor for appropriate treatment regimen for faster recovery. 

We wish you a very healthy & pleasant monsoon season ahead. 

If you have any health related query feel free to share your concern at 
and we will be more than happy to help. 

Saturday 15 April 2023

Hepatitis B - A Vaccine preventable serious Liver Infection

Acute hepatitis B virus infection:

Thirty percent of patients with acute hepatitis B develop icteric hepatitis, while roughly seventy percent have subclinical or anicteric hepatitis. Patients with underlying liver disease or other hepatitis viruses may have a more severe case of the disease.

       One to six months pass during the incubation phase. During the prodromal stage, a syndrome resembling serum sickness may appear, followed by constitutional symptoms, anorexia, nausea, jaundice, and discomfort in the right upper quadrant. In most cases, the symptoms and jaundice go away after one to three months. A rare condition, cute liver failure affects 0.1 to 0.5 percent of patients.

Acute hepatitis with HBsAg positivity can also be diagnosed as: 

(1) Acute hepatitis B

(2) Chronic hepatitis B exacerbations, such as acute hepatitis brought on by drugs and other toxins in a chronic hepatitis B infected person, reactivation of chronic hepatitis B, or superinfection of a chronic hepatitis B infection with hepatitis C, A, E, or D virus.

       Alanine and aspartate aminotransferase levels (ALT and AST) are elevated during the acute phase of acute hepatitis B; values up to 1,000 to 2,000 IU/L are typically seen during this phase, with ALT being higher than AST. The serum levels of lactic dehydrogenase and alkaline phosphatase are typically only slightly elevated (less than threefold). Both the direct and indirect fractions of the bilirubin are variablely elevated. Patients with an-icteric hepatitis may have normal serum bilirubin levels. Except in cases of chronic, severe disease, serum albumin rarely decreases. The best prognosis predictor is the prothrombin time.

        Normalisation of serum aminotransferases takes one to four months to happen in patients who make a full recovery. Persistent elevation of serum ALT for more than six months may indicate progression to chronic hepatitis.

Chronic hepatitis B virus infection:

     The age of infection has a major impact on how quickly acute hepatitis B turns into chronic hepatitis B. The rate is roughly 90% for infections acquired during pregnancy, 20% to 50% for infections acquired between ages one and five, and less than 5% for infections acquired as adults. Hepatitis B virus infection is referred to as chronic if HBsAg is persistently positive for more than six months.

    A thorough history and physical examination with a focus on determining the severity of underlying liver disease and determining treatment eligibility should be performed on people with chronic hepatitis B. Alcohol use, family history of HBV infection, liver disease, and liver cancer, history of complications that would suggest underlying cirrhosis (such as ascites, hematemesis, and mental status changes), and other factors, such as underlying cardiopulmonary disease, past or present psychiatric issues, autoimmune diseases, and other co-morbid conditions, should all be highlighted in the history. Evaluation of advanced liver disease stigmata, such as spider angiomata, palmar erythema, splenomegaly, jaundice, or caput medusa, should be part of a physical examination. Clinicians should be aware, though, that the absence of any one of these findings does not rule out the possibility of underlying cirrhosis. 
    Patients diagnosed with Chronic Hepatitis B should also be mandatorily  screened for HIV and Hepatitis C due to common modes of transmission.

Laboratory Diagnosis : 
   Blood is the preferred specimen, and 3-5 ml of venous blood needs to be drawn and placed in a sterile, dry, and labelled vial. Avoid hemolyzed samples because they might make it difficult for tests to detect markers accurately.
• Within 4 hours of collection, serum from clotted blood should be removed and stored at -20°C to -70°C to prevent the degradation of viral nucleic acid in the specimen.
• Serum samples can be stored for a maximum of 7 days at 4-8°C and  long term storage beyond 7 days should be done at -80 °C. 

Serological markers for Chronic Hepatitis B infection:

1) Hepatitis B surface antigen (HBsAg): 

     After infection, HBV DNA is the first serological marker, followed by HBsAg. Even before the elevation of liver enzymes and the start of a clinical illness, the antigen is detectable. Typically, it goes away 2 months after the start of the clinical illness, but in some cases, such as with chronic infections, it can persist for up to 6 months. Therefore, if this test results in a positive result, the patient is likely contagious, and if it results in a negative result, chronic infection is usually ruled out.

2) Anti-HBsAg (Antibody to HBV surface antigen):

     This antibody manifests when HBsAg is no longer detectable (antibody to HBV surface antigen).It is a protective antibody that shows immunity to HBV from either a prior infection or vaccination.Anti-HBs antibodies have a protective level of 10 mIU/ml.

3) Anti-HBc ( Antibody to HBV core antigen):

       The earliest antibody marker after infection is the anti-HBcIgM (antibody to HBV core antigen). The anti-HBcIgM is the first antibody marker to be detected in blood, appearing in serum a week or two after HBsAg does. Since the anti-HBcIgG antibody may last a lifetime, it serves as a useful marker for previous HBV infection. Total antibody to HBc indicates past or ongoing infection because IgM anti-HBc is only present in acute infections and is replaced by IgG after six months. IgG anti-HBc is a trustworthy indicator of prior HBV infection because it endures even after anti-HBs titers drop to undetectable levels many years following recovery from HBV infection.

4) HBeAg

     In acute, resolving cases, it typically vanishes within a few weeks after appearing in the blood concurrently with or shortly after HBsAg.The presence of this antigen is also used as a criterion for selecting patients for treatment because it is an indicator of active intrahepatic viral replication and, as a result, indicates that the person is highly contagious.Anti-HBe then appears after its disappearance. In the majority of acute hepatitis B cases, testing for HBeAg is not required for routine diagnostic purposes. Instead, individuals in whom HBeAg is a significant marker of viral replication and correlates qualitatively with more quantitative markers of active replication, such as serum HBV DNA detected using molecular techniques, should have their HBeAg levels tested.

  5)Anti-HBeAg :
      It has prognostic implications as the appearance of anti-HBe in acute hepatitis B implies a high likelihood that HBV infection will resolve spontaneously. Anti-HBe's presence in blood denotes low infectivity.

 Serologic markers-caveats:
  •  Precore mutants have mutations in the precore region, which abolishes HBeAg production, or in the core promoter region, which downregulates HBeAg production. Despite possibly producing anti-HBe and anti-HBc antibodies, these patients do not produce HBeAg. 
  • The second group of so-called escape mutants (due to mutations in a determinant of S gene preventing them from being neutralised by the anti-HBs) is seen in some infants born to HBeAg positive mothers and in liver transplant patients who have received combined immunisation with anti-HBV immunoglobulin and vaccine. This has no effect on viral replication; in fact, such cases are more difficult to treat and have a higher risk of turning into cirrhosis. 
  • HBeAg and HBsAg may both be suppressed by co-infection with HCV.
  • HBcAb is occasionally the only serological marker that can be found. This could be either  because of Co-infection with HCV or HIV, Remote infection, "Window" period between HBsAg and HBsAb, False positive test result - HBcAb is marker most prone to false positives or  Resolved HBV with diminishing anti-HBs levels.

 Hepatitis B Occult infection (OBI)

      Viral DNA in blood that is in motion without HBsAg being visible. HBV DNA and anti-HBc would be the only remaining markers after anti-HBe disappears.

Molecular Diagnostics :

 HBV DNA (Quantitative): 

    Hepatitis B DNA PCR is a molecular test that can detect the presence of HBV DNA, which is a marker of viral replication and infectivity like HBeAg.Therefore, HBV DNA is used in clinical practise to track therapy and evaluate patient response to it, such as every three months for years when the patient is taking oral agents and every month for six to twelve months if the patient is taking PEG/IFN. The identification of occult HBV infection is another use for it.

Genotyping and Resistance Testing :

      The genotyping is recommended for both epidemiological purposes in the case of an outbreak investigation and for the detection of mutations that confer resistance to antiviral agents. Eight different HBV genotypes (A to H) have been identified through genotyping of patient isolates. Sequencing and hybridization techniques (Line Probe Assay) are used for genotyping.

Treatment of Chronic Hepatitis B: 

Candidates for treatment -

  • Regardless of ALT levels, HBeAg status, or HBV DNA levels, treatment for all adults, adolescents, and kids with CHB and signs of compensated or decompensated cirrhosis should be prioritised.
  • Regardless of HBeAg status, treatment is advised for adults with CHB who do not have cirrhosis but are older than 30 (in particular), have persistently abnormal ALT levels, and show evidence of high-level HBV replication (HBV DNA >20 000 IU/mL).
Whom NOT to Treat :

  • In people without signs of cirrhosis, with persistently normal ALT levels, and with low levels of HBV replication (HBV DNA 2000 IU/mL), regardless of HBeAg status or age, antiviral therapy is not advised and can be postponed.
  • In the absence of HBV DNA testing, treatment can be postponed in HBeAg-positive people 30 years of age or younger with persistently normal ALT levels.
  • All CHB patients need to be monitored regularly, but it's especially important for those who don't currently fit the guidelines for whether or not to receive treatment, to find out if antiviral therapy will ever be necessary to stop the progression of liver disease. These people include those under 30 years old without cirrhosis who have HBV DNA levels greater than 20,000 IU/mL but persistently normal ALT.

Treatment modalities of Chronic Hepatitis B Infection :

  • The NAs with a high barrier to drug resistance (tenofovir or entecavir) are advised for all adults, adolescents, and children aged 12 years or older for whom antiviral therapy is indicated.
  • Tenofovir may be preferred as the medication of choice in women of childbearing age in the event of pregnancy. Pregnancy is not advised when using entecavir.
  • Patients with a risk of developing Entecavir resistance who have taken lamivudine are advised to use tenofovir instead.
  • Children between the ages of 2 and 11 should not take entecavir.
  • Entecavir may be preferred over Tenofovir in Age > 60, history of fragility fractures or osteoporosis; use of other drugs that worsen bone density, altered renal function (eGFR 60 mL/min/1.73 m2, albuminuria > 30 mg/24 hr, moderate dipstick proteinuria, Low phosphate (2.5 mg/dL) or in patients receiving hemodialysis.
  • Drugs with a low barrier to resistance (lamivudine, adefovir, or telbivudine) are available but not advised as they promote drug resistance. Tenofovir alafenamide fumarate (TAF) is the drug of choice in patients with reduced renal function or bone disease bone toxicities, where entecavir is contraindicated.   
      Prior to, during, and after treatment, CHB patients are monitored for disease progression and treatment response.It is advised that the following be checked at least once a year:
  • HBV DNA levels (where HBV DNA testing is available), HBsAg, HBeAg, and ALT levels (and AST for APRI)
  • Non-invasive tests (APRI score, FIB-4, or FibroScan) to determine whether fibrosis has gotten worse or whether cirrhosis has developed in people who didn't have it at the start.
  • If receiving treatment, adherence needs to be checked frequently and at each appointment.
    Given the risk of reactivation, which can also result in severe acute-on-chronic liver injury, all individuals with cirrhosis based on clinical evidence (or adults with an APRI score >2) require lifelong treatment with NAs.
   Hepatitis B treatment should not typically be stopped without consulting medical professionals with the necessary knowledge, who should be found in specialised facilities.
    When deciding to stop therapy, it is important to carefully weigh the financial impact of continuing to pay for medication and monitoring versus the risk of virological relapse, decompensation, and death. Antiviral treatment should not be stopped for any cirrhotic patients due to the possibility of reactivation, which could result in decompensation and death.


Monday 27 March 2023

Scrub Typhus - A potentially life threatening fever ?

 What is scrub typhus ?

    Orientia tsutsugamushi, an obligate intracellular gram-negative bacterium, is the source of the acute febrile illness known as scrub typhus. Although scrub typhus caused by other Orientia species has been reported in Africa, France, the Middle East, and South America, it is believed to be endemic to the tsutsugamushi triangle, which includes Asia, northern Australia, and islands in the Indian and Pacific Oceans. According to a recent systematic review from hospital-based studies in India, scrub typhus was the root cause of 25% of acute undifferentiated febrile illnesses. 

     O. tsutsugamushi transmitted by the bites of infected chiggars( trombiculid mite) has been linked in recent studies to acute encephalitis syndrome (AES) outbreaks in India, particularly in the northern states of Uttar Pradesh, Bihar, West Bengal, and Assam. Outbreaks of AES pose a major public health problem in India, predominantly affecting children. 

Spectrum of Clinical Features-

      All patients who exhibit an acute onset of fever and altered mental status are included in the broad definition of Acute Encephalitis Syndrome used for syndromic surveillance. Typical clinical features include fever with chills & rigor ,headache,bodyaches,muscle cramps,altered sensorium ,lymphadenopathy and rash .

 The pathognomonic classical scrub typhus rash has been described as a dark scab like region at the site of the chiggar bite, popularly known as 'Eschar'.

      The clinical manifestation may be brought on by encephalitis, meningitis, or encephalopathy without CNS invasion, such as in cases of severe systemic infection, metabolic disturbance, or other neurologic complications following the infection. 

Diagnostic Challenges-

        Early diagnosis is essential for starting prompt, targeted treatment, which can lower scrub typhus complications and fatality rates. Due to the symptoms' similarity to those of other tropical infections that are endemic to the region and can also cause AES, such as dengue, chikungunya, malaria, and leptospirosis, clinical diagnosis can be difficult. 

       There are drawbacks to the current microbiological diagnostics for scrub typhus, which are typically based on IgM detection in serum samples or nucleic acid by PCR. IgM can persist for a long time after the onset of acute illness, and it can react with IgM from other cocirculating pathogens. IgM first appears in serum 5–6 days after the onset of illness .Therefore, it is challenging to determine O. tsutsugamushi as the cause in AES patients who also have microbiological evidence of another potential pathogen.

        Patients with suspected neurologic scrub typhus do not undergo routine IgM detection in cerebrospinal fluid (CSF).The immunofluorescence assay has long been regarded as the gold standard in serologic testing, but its use is constrained by its high cost and difficult interpretation. Serologic tests' limitations in terms of cross-reacting and persistent antibodies may be addressed by PCR, but a positive result is only likely to occur during the bacteremia stage of infection .

        Additionally, blood or eschar material are suggested samples for O. tsutsugamushi PCR, whereas it is unknown how sensitive PCR is to CSF.

          More than 50% of patients had anaemia, leukocytosis, thrombocytopenia, transaminitis, hypoalbuminemia, and uremia. Most patients' CSF tests showed lymphocytic pleocytosis and increased protein concentration.


       Doxycycline 100mg twice daily x 10 days has been the drug of choice for most of the patients without having obvious comorbid conditions. Supportive therapy in terms of Paracetamol, Intravenous Fluids etc are often required. Comorbid conditions like Diabetes Mellitus, Pre-existing Nephropathy can lead to AKI like manifestations in selected group of patients. Hence a constant vigilant monitoring of serum creatinine, electrolytes along with CRP/Procalcitonin  may be of importance to optimise the therapeutic outcome. 

Sunday 5 March 2023

Typhoid vaccine price in India - Know why it is worth the cost

 What is Typhoid Fever ?

    A potentially fatal multisystemic infection known as enteric fever, also known as typhoid fever is caused primarily by Salmonella enterica serotype typhi and, to a lesser extent, paratyphi A, B, and C. ICD 10 code for enteric fever is now A01.00. Salmonella are motile enterobacteriaceae that can cause a number of different gastrointestinal infections. Typhoid, which is primarily caused by Salmonella enterica serotype typhi and, to a lesser extent, S enterica serotypes paratyphi A, B, and C, is the most dangerous of these. From a severe septic illness to minor cases of diarrhoea with low-grade fever, it can present in a wide range of ways. Fever, malaise, diffuse abdominal pain, and constipation are characteristics of the classic presentation. Typhoid fever that is left untreated can lead to delirium, obtundation, intestinal bleeding, bowel perforation, and death in less than a month.

    It has grown more and more resistant to antibiotics over time. Extensively drug-resistant typhoid (XDR) was reported in Pakistan in 2016. Azithromycin, carbapenems, and tigecycline are the only antimicrobial classes that are still effective against these strains.

     Conditions of poor sanitation, overcrowding, and social unrest favour the growth of typhoid.  Typhoid fever is still endemic in developing nations, despite the fact that antibiotics have significantly decreased its prevalence in the developed world. It's possible that S paratyphi infections are becoming more common than S typhi infections. This might be brought on by the immunologic immaturity of a particular population as well as the insufficient protection against these pathogens offered by the current Typhoid vaccines. Most commonly, non-Typhoidal strains cause a mild, self-limiting gastroenteritis. Nevertheless Typhoid vaccines play a crucial role both in primary prevention and decreasing the disease severity in affected individuals.

Vaccines for prevention :

Courtesy : Dr Koushik's Medicare 

        Typhoid fever can be prevented by two vaccinations. The first is a live, attenuated (weakened) vaccine, and the second is an inactivated (dead) vaccine. Which typhoid vaccine is ideal for you can be decided with the aid of your doctor. Typhoid vaccination that has been inactivated is given by injection. Children of 2 years of age and older may receive it. At least two weeks prior to departure, one dose is advised. For those who continue to be at danger, repeated doses every two years are advised.

        Oral live typhoid vaccine administration (by mouth). Six years of age and older individuals may receive it. Every other day, one capsule is taken, making a total of four capsules. At least a week before departure, the last dose should be taken.About an hour before meals, each capsule should be taken whole (without chewing) with cold or lukewarm water. For those who continue to be at risk, a booster shot is required every five years. It's crucial to keep live typhoid vaccine capsules chilled (not frozen).

      In developed countries  most of the time routine typhoid immunisation is not advised, although the following situations may warrant administration of typhoid vaccines.

a) Tourists going to regions where typhoid is widespread. (NOTE: Typhoid vaccination is not 100% effective and is not a replacement for exercising caution while choosing foods and beverages.)

b) Individuals in close proximity to a typhoid carrier.

c) Employees in laboratories that handle Salmonella typhi bacterial culture and strains

The typhoid vaccine may be administered concurrently with other shots.

     In 2023 typhoid vaccine price in India is around INR 1500-2500 based on the brands available. You can check the same on : https://www.apollopharmacy.in/medicine/typbar-tcv-pfs-injection-0-5ml

     Typbar TCV Vaccine 0.5 ml. It includes sodium chloride and the purified Vi polysaccharide typhoid vaccine. Typhoid disease is prevented with it. A non-toxic and safe form of the causative bacteria's capsular specimen is injected into the body by Typbar TCV Vaccine, which prompts the body to produce antibodies and confers immunity. The body keeps track of this immune response to ensure that it is ready in the event that these bacteria invade again in the future.

Friday 24 February 2023

Difficult to Treat Infections ? Take a look

     Antibiotics have been a wonderful invention in the evolution of modern medical treatments. The mortality and the morbidity due to different infectious diseases have remarkably gone down over the last many decades. However pathogens have emerged as even more smarter than mankind developing different complex resistance mechanisms to survive the assault of antibiotics thereby rendering treatment of infectious diseases a difficult challenge. Patients with Diabetic Ketoacidosis, Chronic Renal failure, Implants & Prosthesis often land up with sepsis with multi drug resistant organisms ,treatment of which pose a serious challenge to the treating clinicians. To combat this crisis, antibiotic stewardship practice has become the need of the hour which emphasize the rational & judicious use of all available antibiotics. The regulatory authority should be more vigilant in preventing the over the counter dispensing of antibiotics.

     Having said that, all the medical fraternities and academic forums should take initiatives to implement antibiotic stewardship practices in day to day clinical practices. Let us have a quick brush up of the antibiotic resistance mechanisms.   


    Due to an increase in community-acquired infections, ESBL-E has become more frequently detected in bacterial cultures.The majority of penicillins, cephalosporins, and aztreonam are rendered inactive by ESBL enzymes. Carbapenems continue to generally be effective against EBSL-E. ESBLs do not render non-lactam agents inactive (e.g., ciprofloxacin, trimethoprim-sulfamethoxazole, gentamicin). However, organisms with ESBL genes frequently have extra genes or gene mutations that cause resistance to a variety of antibiotics. 

     Although ESBL genes can be found in any Gram-negative organism, Escherichia coli, Klebsiella pneumoniae, Klebsiella oxytoca, and Proteus mirabilis have the highest rates of occurrence. The most widespread CTX-M enzymes are CTX-M-15. Other ESBLs with distinctive hydrolyzing properties exist in addition to CTX-M enzymes, such as variants of narrow-spectrum TEM and SHV -lactamases with amino acid substitutions, though they have undergone less thorough clinical testing. Most clinical microbiology laboratories don't conduct routine EBSL testing. Although this threshold has limitations with specificity because organisms that are not susceptible to ceftriaxone for reasons other than ESBL production may be mistakenly assumed to be ESBL-producers, non-susceptibility to ceftriaxone (i.e., ceftriaxone minimum inhibitory concentrations [MICs] 2 mcg/mL) is frequently used as a proxy for ESBL production.


      Members of the Enterobacterales order who are resistant to at least one carbapenem antibiotic or who produce a carbapenemase enzyme are known as CRE, according to the CDC .Resistance to at least one carbapenem other than imipenem is necessary for bacteria that are inherently resistant to imipenem (such as Proteus spp., Morganella spp., and Providencia spp.). The pathogens that cause CRE can be roughly divided into those that produce carbapenemase and those that do not into groups with different potential mechanisms of resistance. The amplification of non-carbapenemase -lactamase genes (other than carbapenemase genes) with concurrent outer membrane porin disruption may cause CRE that do not produce carbapenemase. 35% to 59% of CRE cases in the US are caused by isolates that produce carbapenemase.

    K. pneumoniae carbapenemases (KPCs), which can be produced by any Enterobacterales, are the most prevalent carbapenemases. The Verona integron-encoded metallo-lactamases (VIMs), imipenem-hydrolyzing metallo-lactamases (IMPs), and oxacillinases (such as OXA-48-like) are additional notable carbapenemases that have been discovered . Making treatment decisions requires having knowledge of whether a CRE clinical isolate produces carbapenemase and, if so, what kind of carbapenemase is produced.

    CRE that produce carbapenemase and those that do not can be distinguished by phenotypic tests like the modified carbapenem inactivation method and the Carba NP test. Molecular analysis can pinpoint particular carbapenemase families (e.g., differentiating a KPC from an OXA-48-like carbapenemase). A small number of clinical microbiology laboratories perform carbapenemase phenotypic and/or genotypic testing, but most of the international bodies strongly encourage all clinical microbiology laboratories to pursue carbapenemase testing in order to guide the best possible treatment choices. The following treatment suggestions for CRE infections presuppose that preferred and alternative antibiotics have shown in vitro activity.

MDR/DTR Pseudomonus aeruginosa:

 Penicillins, cephalosporins, fluoroquinolones, aminoglycosides, and carbapenems are among the antibiotic classes for which P. aeruginosa susceptibility is typically anticipated. MDR P. aeruginosa is defined as P. aeruginosa not susceptible to at least one antibiotic in at least three antibiotic classes . The idea of "difficult-to-treat" resistance was put forth in 2018. DTR is defined  as P. aeruginosa that does not exhibit sensitivity to any of the following drugs: piperacillin-tazobactam, ceftazidime, cefepime, aztreonam, meropenem, imipenem-cilastatin, ciprofloxacin, and levofloxacin.

Multidrug-resistant P. aeruginosa, also known as DTR-P. aeruginosa, typically arises from the interaction of several complex resistance mechanisms, such as reduced expression of outer membrane porins (OprD), increased production of AmpC enzymes, increased activity of efflux pumps, and mutations in targets of the penicillin-binding protein . Carbapenemase production is a rare cause of carbapenem resistance in P. aeruginosa, but it has been found in up to 20% of carbapenem-resistant P. aeruginosa worldwide.

Table . Suggested dosing of antibiotics for the treatment of infections caused by antimicrobial- resistant organisms

Reference : Infectious Disease Society of America (IDSA)




Adult Dosage

(assuming normal renal and liver function )


Target Organisms 


Cystitis: 15 mg/kg/dose  IV once

All other infections: 20 mg/kg/dose  IV x 1 dose, subsequent doses and dosing interval based on pharmacokinetic evaluation


P. aeruginosa


9 g IV q8h over 4 hours OR 27 g IV q24h as a continuous infusion

For mild infections caused by CRAB isolates susceptible to ampicillin-sulbactam, it is reasonable to administer 3g IV q4h

particularly if intolerance or toxicities preclude the use of higher dosages.



Cystitis: 1 g IV q8h

All other infections: 2 g IV q8h, infused over 3 hours



2 g IV q8h, infused over 3 hours

CRE, DTR-P. aeruginosa, CRAB, S. maltophilia

Ceftazidime- avibactam

2.5 g IV q8h, infused over 3 hours

CRE, DTR-P. aeruginosa

Ceftazidime- avibactam and aztreonam

Ceftazidime-avibactam: 2.5 g IV q8h, infused over 3 hours


Aztreonam: 2 g IV q8h, infused over 3 hours, administered at the same time as ceftazidime-avibactam, if possible

Metallo-β-lactamase- producing CRE, S. maltophilia

Ceftolozane- tazobactam

Cystitis: 1.5 g IV q8h, infused over 1 hour

All other infections: 3 g IV q8h, infused over 3 hours

DTR-P. aeruginosa


ESBL-E or AmpC infections: 400 mg IV q8h-q12h OR 500 – 750 mg PO q12h



Refer to international consensus guidelines on polymyxins 

CRE cystitis, DTR-P. aeruginosa cystitis, CRAB cystitis


1 mg/kg/dose IV q12h



1 g IV q24h, infused over 30 minutes



Cystitis: 3 g PO x 1 dose

ESBL-E. coli cystitis



Adult Dosage

(assuming normal renal and liver function )


Target Organisms 


Cystitis: 5 mg/kg/dose  IV once

All other infections: 7 mg/kg/dose  IV x 1 dose, subsequent doses and dosing interval based on pharmacokinetic evaluation


DTR-P. aeruginosa


Cystitis (standard infusion): 500 mg IV q6h, infused over 30 minutes

All other ESBL-E or AmpC-E infections: 500 mg IV q6h, infused over 30 minutes

All other CRE and CRAB infections: 500 mg IV q6h, infused over 3 hours


Imipenem-cilastatin- relebactam

1.25 g IV q6h, infused over 30 minutes

CRE, DTR-P. aeruginosa


750 mg IV/PO q24h

ESBL-E, AmpC-E, S.



Cystitis (standard infusion): 1 g IV q8h, infused over 30 minutes

All other ESBL-E or AmpC-E infections: 1-2 g IV q8h, infused over 30 minutes

All other CRE and CRAB infections: 2 g IV q8h, infused over 3 hours


Meropenem- vaborbactam

4 g IV q8h, infused over 3 hours



200 mg IV/PO q12h

CRAB, S. maltophilia


Cystitis: Macrocrystal/monohydrate (Macrobid®) 100 mg PO q12h

Cystitis: Oral suspension: 50 mg PO q6h

ESBL-E cystitis, AmpC-E cystitis


Cystitis: 15 mg/kg IV x 1 dose

All other infections: 15 mg/kg IV x 1 dose, subsequent doses and dosing interval based on pharmacokinetic evaluation


DTR-P. aeruginosa

Polymyxin B

Refer to international consensus guidelines on polymyxins 

DTR-P. aeruginosa, CRAB


200 mg IV x 1 dose, then 100 mg IV q12h

CRE, CRAB, S. maltophilia




Adult Dosage

(assuming normal renal and liver function )


Target Organisms 


Cystitis: 5 mg/kg/dose IV x 1 dose

All other infections: 7 mg/kg/dose IV x 1 dose; subsequent doses and dosing interval based on pharmacokinetic evaluation


DTR-P. aeruginosa

Trimethoprim- sulfamethoxazole

Cystitis: 160 mg (trimethoprim component) IV/PO q12h

Other infections: 8-12 mg/kg/day (trimethoprim component) IV/PO divided q8-12h (consider maximum dose of 960 mg trimethoprim component per day)

ESBL-E, AmpC-E, S.


AmpC-E: AmpC β-lactamase-producing Enterobacterales; CRAB: Carbapenem-resistant Acinetobacter baumannii; CRE: Carbapenem-resistant Enterobacterales; DTR-P. aeruginosa: Pseudomonas aeruginosa with difficult-to-treat resistance; E. coli: Escherichia coli; ESBL-E: Extended-spectrum β-lactamase-producing Enterobacterales; IV: Intravenous; MIC: Minimum inhibitory concentration; PO: By mouth; q4h: Every 4 hours; q6h: Every 6 hours; q8h: Every 8 hours; q12h: Every 12 hours; q24h: Every 24 hours; S. maltophilia: Stenotrophomonas maltophilia