This document discusses Streptococci and Enterococci bacteria. It begins by classifying streptococci based on their hemolytic patterns on blood agar plates and Lancefield cell wall antigen groups. It then discusses specific pathogenic streptococci species found in humans, including their Lancefield groups and hemolytic properties. Some zoonotic streptococci species are also mentioned. The document concludes by presenting three clinical cases involving Group A streptococcus (Streptococcus pyogenes), necrotizing fasciitis, and Streptococcus pneumoniae.
This document discusses the genus Streptococcus. It describes streptococci as gram-positive cocci that are facultative anaerobes and ferment carbohydrates producing lactic acid. It classifies streptococci based on their hemolytic properties and discusses important pathogenic species like Streptococcus pyogenes. It also covers virulence factors of S. pyogenes like M protein and streptolysin toxins. Common infections caused by streptococci like pharyngitis and impetigo are mentioned along with post-infectious complications like rheumatic fever and glomerulonephritis.
Acute rheumatic fever is an immune-mediated disease that can develop weeks after a Group A streptococcal throat infection. It commonly affects the heart, joints, skin, and brain in children ages 5-15. The disease is caused by an abnormal immune response to the bacterial infection. Symptoms may include migratory arthritis, heart inflammation (carditis), abnormal movements (chorea), and skin nodules or rashes. Diagnosis is based on the modified Jones criteria and treatment involves antibiotics, anti-inflammatories, and long-term prevention of recurrent episodes through antibiotics. Untreated, it can lead to permanent heart valve damage known as rheumatic heart disease.
This document discusses rheumatic heart disease, which is a chronic condition that develops due to damage caused by acute rheumatic fever during childhood. Rheumatic fever is an inflammatory disease that occurs after a streptococcal throat infection and can cause long-term heart valve problems and scarring referred to as rheumatic heart disease. It most often affects the mitral valve and is characterized by narrowed or leaky valves. Treatment involves antibiotics to prevent recurrence, as well as medications and potentially surgery to address heart failure and valve abnormalities.
DENGUE - classification, symptoms and treatmentmansipatel951
Dengue is a prevalent arthropod-borne viral disease affecting over 100 million people annually. It is transmitted by Aedes aegypti and Aedes albopictus mosquitoes. There are four serotypes of the dengue virus that cause illness. Symptoms include fever, headache, muscle and joint pains, and bleeding manifestations. Secondary infection with a different serotype increases the risk of developing severe dengue, characterized by plasma leakage, fluid accumulation, bleeding, and organ impairment. Treatment focuses on fluid replacement and management of warning signs such as abdominal pain and vomiting.
Neonatal sepsis is a blood infection in infants under 90 days old that is a major cause of neonatal mortality. It can be caused by various bacteria, viruses, fungi or parasites. The presentation may include non-specific symptoms like temperature instability or feeding difficulties. Treatment involves supportive care and antibiotics, with a focus on early detection and treatment to prevent severe complications or death, which occurs in 13-25% of cases without timely intervention. Risk factors include prematurity, maternal infections, and improper sanitation or medical techniques.
Rheumatic heart disease is a chronic condition caused by rheumatic fever, which is triggered by an autoimmune reaction to a group A streptococcal infection. It most commonly affects the mitral valve, causing inflammation and scarring that can lead to valvular problems like stenosis or regurgitation. In developing countries, rheumatic heart disease remains a major public health problem, with over 15 million cases worldwide resulting in over 200,000 deaths annually. Treatment involves antibiotics to treat the initial strep infection along with medications and potentially surgery to address valvular damage.
This document discusses fever, pyrexia of unknown origin (PUO), and systemic inflammatory response syndrome (SIRS). It provides definitions and differential diagnoses for fever and PUO. Two case scenarios are presented: a 15-year-old girl with new onset fever and symptoms, and a 51-year-old woman with jaundice and weight loss. Key aspects to consider in the history, examination, investigations, and management of patients with fever are outlined. Common causes of fever and appropriate first-line antibiotic choices are also listed.
Rheumatic fever is an autoimmune disease that can develop after a streptococcal throat infection. It causes inflammation in various body systems like the heart, joints, brain and skin. The pathogenesis involves antibodies produced against streptococci that cross-react with human tissues due to molecular mimicry. Rheumatic fever is diagnosed using the modified Jones criteria and treated with antibiotics to eliminate the streptococcal infection as well as anti-inflammatory drugs. Long-term prevention involves continued antibiotic prophylaxis to prevent recurrent attacks that can lead to chronic rheumatic heart disease.
This document discusses the genus Streptococcus. It describes streptococci as gram-positive cocci that are facultative anaerobes and ferment carbohydrates producing lactic acid. It classifies streptococci based on their hemolytic properties and discusses important pathogenic species like Streptococcus pyogenes. It also covers virulence factors of S. pyogenes like M protein and streptolysin toxins. Common infections caused by streptococci like pharyngitis and impetigo are mentioned along with post-infectious complications like rheumatic fever and glomerulonephritis.
Acute rheumatic fever is an immune-mediated disease that can develop weeks after a Group A streptococcal throat infection. It commonly affects the heart, joints, skin, and brain in children ages 5-15. The disease is caused by an abnormal immune response to the bacterial infection. Symptoms may include migratory arthritis, heart inflammation (carditis), abnormal movements (chorea), and skin nodules or rashes. Diagnosis is based on the modified Jones criteria and treatment involves antibiotics, anti-inflammatories, and long-term prevention of recurrent episodes through antibiotics. Untreated, it can lead to permanent heart valve damage known as rheumatic heart disease.
This document discusses rheumatic heart disease, which is a chronic condition that develops due to damage caused by acute rheumatic fever during childhood. Rheumatic fever is an inflammatory disease that occurs after a streptococcal throat infection and can cause long-term heart valve problems and scarring referred to as rheumatic heart disease. It most often affects the mitral valve and is characterized by narrowed or leaky valves. Treatment involves antibiotics to prevent recurrence, as well as medications and potentially surgery to address heart failure and valve abnormalities.
DENGUE - classification, symptoms and treatmentmansipatel951
Dengue is a prevalent arthropod-borne viral disease affecting over 100 million people annually. It is transmitted by Aedes aegypti and Aedes albopictus mosquitoes. There are four serotypes of the dengue virus that cause illness. Symptoms include fever, headache, muscle and joint pains, and bleeding manifestations. Secondary infection with a different serotype increases the risk of developing severe dengue, characterized by plasma leakage, fluid accumulation, bleeding, and organ impairment. Treatment focuses on fluid replacement and management of warning signs such as abdominal pain and vomiting.
Neonatal sepsis is a blood infection in infants under 90 days old that is a major cause of neonatal mortality. It can be caused by various bacteria, viruses, fungi or parasites. The presentation may include non-specific symptoms like temperature instability or feeding difficulties. Treatment involves supportive care and antibiotics, with a focus on early detection and treatment to prevent severe complications or death, which occurs in 13-25% of cases without timely intervention. Risk factors include prematurity, maternal infections, and improper sanitation or medical techniques.
Rheumatic heart disease is a chronic condition caused by rheumatic fever, which is triggered by an autoimmune reaction to a group A streptococcal infection. It most commonly affects the mitral valve, causing inflammation and scarring that can lead to valvular problems like stenosis or regurgitation. In developing countries, rheumatic heart disease remains a major public health problem, with over 15 million cases worldwide resulting in over 200,000 deaths annually. Treatment involves antibiotics to treat the initial strep infection along with medications and potentially surgery to address valvular damage.
This document discusses fever, pyrexia of unknown origin (PUO), and systemic inflammatory response syndrome (SIRS). It provides definitions and differential diagnoses for fever and PUO. Two case scenarios are presented: a 15-year-old girl with new onset fever and symptoms, and a 51-year-old woman with jaundice and weight loss. Key aspects to consider in the history, examination, investigations, and management of patients with fever are outlined. Common causes of fever and appropriate first-line antibiotic choices are also listed.
Rheumatic fever is an autoimmune disease that can develop after a streptococcal throat infection. It causes inflammation in various body systems like the heart, joints, brain and skin. The pathogenesis involves antibodies produced against streptococci that cross-react with human tissues due to molecular mimicry. Rheumatic fever is diagnosed using the modified Jones criteria and treated with antibiotics to eliminate the streptococcal infection as well as anti-inflammatory drugs. Long-term prevention involves continued antibiotic prophylaxis to prevent recurrent attacks that can lead to chronic rheumatic heart disease.
This 8-year-old cat presented with a 6-week history of sneezing and 1-week history of right-sided facial swelling. Diagnostic testing revealed chronic kidney disease, hyperglobulinemia, and neutrophilia. CT imaging showed a soft tissue mass filling the right nasal cavity and bone lysis. Rhinoscopy and nasal biopsies found marked neutrophilic rhinitis on the right and mild rhinitis on the left, with no evidence of neoplasia or fungi. Abdominal ultrasound showed shrunken kidneys consistent with chronic kidney disease. The facial swelling is likely due to a chronic, non-neoplastic rhinitis, though a secondary bacterial infection cannot be ruled out
This document discusses dengue, a mosquito-borne viral disease. It causes a flu-like illness called dengue fever or a potentially lethal complication called dengue hemorrhagic fever/dengue shock syndrome. The causative agent is one of four dengue virus serotypes transmitted by Aedes mosquitoes. Symptoms include fever, rash and bleeding. Diagnosis involves detecting virus, viral antigens or antibodies. Treatment focuses on fluid replacement and supportive care. Prevention relies on mosquito control measures. Secondary infection with a different serotype increases the risk of severe disease due to antibody-dependent enhancement.
- An 18-month old female Savannah cat presented with 2 weeks of progressive ataxia and reduced appetite. Physical examination revealed vestibular syndrome and pyrexia. Bloodwork and additional testing ruled out several potential causes. Abdominal ultrasound found an effusion that tested positive for feline coronavirus via PCR. Despite negative coronavirus results on the fluid, FIP remained the most likely diagnosis given the signalment, clinical signs, and fluid analysis findings. The cat was started on remdesivir and showed rapid neurological improvement, supporting a presumptive diagnosis of FIP.
- Acute rheumatic fever is an autoimmune disease that develops after a streptococcal infection. It can cause inflammation in joints, heart valves, brain, and skin.
- The document discusses the etiology, pathogenesis, clinical features, and management of acute rheumatic fever. It is caused by an immune reaction to a streptococcal infection that results in cross-reactivity with human tissues. Common symptoms include polyarthritis, carditis, chorea, and erythema marginatum.
- Diagnosis involves confirming a preceding streptococcal infection through elevated antibody titers as well as evidence of systemic inflammation from tests like ESR and CRP. Echocardiography and ECG can
bacterial infection part 2 and about their managments.pptxBekaluTemesgen2
Shigellosis is an acute infectious inflammatory colitis caused by Shigella species, transmitted via the fecal-oral route. It presents with fever and frequent, bloody diarrhea, and can lead to complications like toxic megacolon. Diagnosis is made via stool culture or detection of Shiga toxins. Treatment involves oral rehydration and antibiotics. Prevention relies on good environmental hygiene and handwashing.
Salmonellosis is caused by Salmonella species, transmitted via contaminated food or water. Typhoid fever is a systemic infection caused by S. Typhi and S. Paratyphi. It presents with fever and gastrointestinal or systemic symptoms. Diagnosis involves blood or bone marrow cultures.
This document discusses acute encephalitis syndrome. It defines encephalitis as an acute inflammatory process involving brain tissue and meningoencephalitis as inflammation of both the meninges and brain tissue. Japanese encephalitis is identified as one of the most common causes of acute encephalitis syndrome. It is a mosquito-borne viral infection spread between pigs and birds as amplifying hosts, with humans as incidental hosts. The clinical presentation involves an initial prodromal stage of fever and headache, followed by an encephalitic stage with altered mental status such as confusion or coma. Treatment involves supportive care and empiric antiviral therapy with acyclovir and antibiotics until causative organisms are identified.
This document provides information about immunization and vaccine-preventable diseases. It discusses:
1. Immunization is a process that uses vaccines to stimulate immunity against infectious diseases. It has proven effective at controlling and eliminating diseases like smallpox.
2. Major vaccine-preventable diseases that kill children include measles, polio, pertussis, Hib, and pneumococcal diseases. Immunization is one of the most cost-effective health interventions.
3. The document then provides details on specific diseases like pertussis, its symptoms, complications, and treatment with antibiotics or immunization. It emphasizes the importance of clinical diagnosis and avoiding severe outcomes in infants.
This document discusses central nervous system (CNS) infections, including:
- Viral infections are more common than bacterial, which are more common than fungal/parasitic. Rickettsiae and Mycoplasma can also cause CNS infections.
- There are three main types - meningitis, encephalitis, and meningioencephalitis.
- Meningitis can be caused by bacteria, viruses, fungi or parasites. Presentation depends on age. Encephalitis has multiple viral and non-viral causes. Meningioencephalitis involves both meninges and brain tissue.
Complications, diagnosis, and management are discussed for each type of infection.
Rheumatic heart disease is caused by rheumatic fever, which results from a streptococcal throat infection. It often affects children in developing countries. Rheumatic fever causes inflammation that damages the heart valves over time, leading to permanent valve problems. The mitral valve is most often affected, resulting in complications like murmurs, cardiomegaly, and cardiac failure. Diagnosis involves assessing for symptoms of previous streptococcal infection and valvular damage, along with lab tests and echocardiogram. Treatment focuses on antibiotics to prevent future infections from triggering relapses, as well as medications and potentially surgery to address valvular problems.
Interactive talk on common hematological and oncological emergencies - which if not noticed early can lead to irreversible complications and death .
Intended to be used for educational purposes for the fertile minds in medicine .
This document discusses viral hepatitis, focusing on hepatitis A, B, C, D, and E viruses. It provides details on the structure and transmission of each virus. It also summarizes the typical clinical progression and serological markers of acute and chronic infection for each virus type. The diagnosis, treatment, and complications of viral hepatitis infections are outlined.
This document provides information on Neisseria meningitidis, the bacteria that causes meningococcal meningitis. It describes the morphology and virulence factors of N. meningitidis, including its capsular polysaccharide and outer membrane proteins. The epidemiology, transmission, pathogenesis, clinical features, diagnosis and treatment of meningococcal meningitis are discussed in detail. Serious complications like meningococcemia and Waterhouse-Friderichsen syndrome are also summarized.
This document provides an overview of dengue fever, including:
1. It describes the dengue virus, its vector Aedes aegypti mosquito, and the disease's pathogenesis and clinical presentations ranging from mild dengue fever to severe dengue hemorrhagic fever and dengue shock syndrome.
2. It outlines the laboratory diagnosis and management approach divided into three groups - outpatient, inpatient, and emergency treatment groups.
3. It discusses treatment approaches for different clinical stages of the disease as well as vector control methods and the status of vaccine development.
Rheumatic fever is an autoimmune disease that can develop as a result of a streptococcal throat infection. It causes inflammation of the heart, joints, brain, and skin. The disease is most common in children ages 5-15 in developing countries. It is diagnosed using the Modified Jones Criteria which looks for major criteria like heart inflammation, arthritis, subcutaneous nodules, and minor criteria like fever and joint pain along with evidence of a prior streptococcal infection. Treatment involves antibiotics to treat the infection as well as medications for symptoms while long term prevention relies on regular antibiotics.
A brief discussion of a very common bacterial infection presenting as fever and skin rash following skin infection or use of tampons. Affecting adults especially women. Very helpful for medical students, ER doctors, dermatologists, nurses. References from dermatology textbook Rooks.
This document summarizes several tick-borne and zoonotic diseases, including their causative agents, vectors, clinical manifestations, diagnosis, and treatment. Granulocytic anaplasmosis is caused by Anaplasma phagocytophilum, transmitted by Ixodes ticks, and presents as fever, myalgia and leukopenia. Ehrlichiosis is caused by Ehrlichia species and presents as nonspecific symptoms like headache and fatigue. Bartonella species cause cat scratch disease from contact with cats, presenting as lymphadenopathy.
This document provides an overview of systemic bacteriology, focusing on important bacterial pathogens like Staphylococcus aureus, Streptococcus pyogenes, and Streptococcus agalactiae. It describes their characteristics, virulence factors, diseases caused, and methods for laboratory diagnosis. Key points covered include S. aureus causing diseases ranging from skin infections to toxic shock syndrome, S. pyogenes causing conditions like strep throat and impetigo as well as non-suppurative sequelae, and S. agalactiae being an important cause of infections in newborn infants. The goal of systemic bacteriology is to improve understanding of bacterial pathogens, the diseases they cause, and approaches for diagnosis, treatment and prevention.
This document provides information about enteric (typhoid) fever, including:
- It is caused by the bacterium Salmonella enterica and is a global public health problem affecting millions annually.
- Clinical features include prolonged high fever, abdominal discomfort, diarrhea or constipation, and potential complications like intestinal perforation.
- Diagnosis involves blood, stool, or bone marrow cultures and serologic tests. Ceftriaxone is the treatment of choice for multidrug-resistant cases. Early diagnosis and appropriate antibiotic treatment are important to prevent complications.
This 8-year-old cat presented with a 6-week history of sneezing and 1-week history of right-sided facial swelling. Diagnostic testing revealed chronic kidney disease, hyperglobulinemia, and neutrophilia. CT imaging showed a soft tissue mass filling the right nasal cavity and bone lysis. Rhinoscopy and nasal biopsies found marked neutrophilic rhinitis on the right and mild rhinitis on the left, with no evidence of neoplasia or fungi. Abdominal ultrasound showed shrunken kidneys consistent with chronic kidney disease. The facial swelling is likely due to a chronic, non-neoplastic rhinitis, though a secondary bacterial infection cannot be ruled out
This document discusses dengue, a mosquito-borne viral disease. It causes a flu-like illness called dengue fever or a potentially lethal complication called dengue hemorrhagic fever/dengue shock syndrome. The causative agent is one of four dengue virus serotypes transmitted by Aedes mosquitoes. Symptoms include fever, rash and bleeding. Diagnosis involves detecting virus, viral antigens or antibodies. Treatment focuses on fluid replacement and supportive care. Prevention relies on mosquito control measures. Secondary infection with a different serotype increases the risk of severe disease due to antibody-dependent enhancement.
- An 18-month old female Savannah cat presented with 2 weeks of progressive ataxia and reduced appetite. Physical examination revealed vestibular syndrome and pyrexia. Bloodwork and additional testing ruled out several potential causes. Abdominal ultrasound found an effusion that tested positive for feline coronavirus via PCR. Despite negative coronavirus results on the fluid, FIP remained the most likely diagnosis given the signalment, clinical signs, and fluid analysis findings. The cat was started on remdesivir and showed rapid neurological improvement, supporting a presumptive diagnosis of FIP.
- Acute rheumatic fever is an autoimmune disease that develops after a streptococcal infection. It can cause inflammation in joints, heart valves, brain, and skin.
- The document discusses the etiology, pathogenesis, clinical features, and management of acute rheumatic fever. It is caused by an immune reaction to a streptococcal infection that results in cross-reactivity with human tissues. Common symptoms include polyarthritis, carditis, chorea, and erythema marginatum.
- Diagnosis involves confirming a preceding streptococcal infection through elevated antibody titers as well as evidence of systemic inflammation from tests like ESR and CRP. Echocardiography and ECG can
bacterial infection part 2 and about their managments.pptxBekaluTemesgen2
Shigellosis is an acute infectious inflammatory colitis caused by Shigella species, transmitted via the fecal-oral route. It presents with fever and frequent, bloody diarrhea, and can lead to complications like toxic megacolon. Diagnosis is made via stool culture or detection of Shiga toxins. Treatment involves oral rehydration and antibiotics. Prevention relies on good environmental hygiene and handwashing.
Salmonellosis is caused by Salmonella species, transmitted via contaminated food or water. Typhoid fever is a systemic infection caused by S. Typhi and S. Paratyphi. It presents with fever and gastrointestinal or systemic symptoms. Diagnosis involves blood or bone marrow cultures.
This document discusses acute encephalitis syndrome. It defines encephalitis as an acute inflammatory process involving brain tissue and meningoencephalitis as inflammation of both the meninges and brain tissue. Japanese encephalitis is identified as one of the most common causes of acute encephalitis syndrome. It is a mosquito-borne viral infection spread between pigs and birds as amplifying hosts, with humans as incidental hosts. The clinical presentation involves an initial prodromal stage of fever and headache, followed by an encephalitic stage with altered mental status such as confusion or coma. Treatment involves supportive care and empiric antiviral therapy with acyclovir and antibiotics until causative organisms are identified.
This document provides information about immunization and vaccine-preventable diseases. It discusses:
1. Immunization is a process that uses vaccines to stimulate immunity against infectious diseases. It has proven effective at controlling and eliminating diseases like smallpox.
2. Major vaccine-preventable diseases that kill children include measles, polio, pertussis, Hib, and pneumococcal diseases. Immunization is one of the most cost-effective health interventions.
3. The document then provides details on specific diseases like pertussis, its symptoms, complications, and treatment with antibiotics or immunization. It emphasizes the importance of clinical diagnosis and avoiding severe outcomes in infants.
This document discusses central nervous system (CNS) infections, including:
- Viral infections are more common than bacterial, which are more common than fungal/parasitic. Rickettsiae and Mycoplasma can also cause CNS infections.
- There are three main types - meningitis, encephalitis, and meningioencephalitis.
- Meningitis can be caused by bacteria, viruses, fungi or parasites. Presentation depends on age. Encephalitis has multiple viral and non-viral causes. Meningioencephalitis involves both meninges and brain tissue.
Complications, diagnosis, and management are discussed for each type of infection.
Rheumatic heart disease is caused by rheumatic fever, which results from a streptococcal throat infection. It often affects children in developing countries. Rheumatic fever causes inflammation that damages the heart valves over time, leading to permanent valve problems. The mitral valve is most often affected, resulting in complications like murmurs, cardiomegaly, and cardiac failure. Diagnosis involves assessing for symptoms of previous streptococcal infection and valvular damage, along with lab tests and echocardiogram. Treatment focuses on antibiotics to prevent future infections from triggering relapses, as well as medications and potentially surgery to address valvular problems.
Interactive talk on common hematological and oncological emergencies - which if not noticed early can lead to irreversible complications and death .
Intended to be used for educational purposes for the fertile minds in medicine .
This document discusses viral hepatitis, focusing on hepatitis A, B, C, D, and E viruses. It provides details on the structure and transmission of each virus. It also summarizes the typical clinical progression and serological markers of acute and chronic infection for each virus type. The diagnosis, treatment, and complications of viral hepatitis infections are outlined.
This document provides information on Neisseria meningitidis, the bacteria that causes meningococcal meningitis. It describes the morphology and virulence factors of N. meningitidis, including its capsular polysaccharide and outer membrane proteins. The epidemiology, transmission, pathogenesis, clinical features, diagnosis and treatment of meningococcal meningitis are discussed in detail. Serious complications like meningococcemia and Waterhouse-Friderichsen syndrome are also summarized.
This document provides an overview of dengue fever, including:
1. It describes the dengue virus, its vector Aedes aegypti mosquito, and the disease's pathogenesis and clinical presentations ranging from mild dengue fever to severe dengue hemorrhagic fever and dengue shock syndrome.
2. It outlines the laboratory diagnosis and management approach divided into three groups - outpatient, inpatient, and emergency treatment groups.
3. It discusses treatment approaches for different clinical stages of the disease as well as vector control methods and the status of vaccine development.
Rheumatic fever is an autoimmune disease that can develop as a result of a streptococcal throat infection. It causes inflammation of the heart, joints, brain, and skin. The disease is most common in children ages 5-15 in developing countries. It is diagnosed using the Modified Jones Criteria which looks for major criteria like heart inflammation, arthritis, subcutaneous nodules, and minor criteria like fever and joint pain along with evidence of a prior streptococcal infection. Treatment involves antibiotics to treat the infection as well as medications for symptoms while long term prevention relies on regular antibiotics.
A brief discussion of a very common bacterial infection presenting as fever and skin rash following skin infection or use of tampons. Affecting adults especially women. Very helpful for medical students, ER doctors, dermatologists, nurses. References from dermatology textbook Rooks.
This document summarizes several tick-borne and zoonotic diseases, including their causative agents, vectors, clinical manifestations, diagnosis, and treatment. Granulocytic anaplasmosis is caused by Anaplasma phagocytophilum, transmitted by Ixodes ticks, and presents as fever, myalgia and leukopenia. Ehrlichiosis is caused by Ehrlichia species and presents as nonspecific symptoms like headache and fatigue. Bartonella species cause cat scratch disease from contact with cats, presenting as lymphadenopathy.
This document provides an overview of systemic bacteriology, focusing on important bacterial pathogens like Staphylococcus aureus, Streptococcus pyogenes, and Streptococcus agalactiae. It describes their characteristics, virulence factors, diseases caused, and methods for laboratory diagnosis. Key points covered include S. aureus causing diseases ranging from skin infections to toxic shock syndrome, S. pyogenes causing conditions like strep throat and impetigo as well as non-suppurative sequelae, and S. agalactiae being an important cause of infections in newborn infants. The goal of systemic bacteriology is to improve understanding of bacterial pathogens, the diseases they cause, and approaches for diagnosis, treatment and prevention.
This document provides information about enteric (typhoid) fever, including:
- It is caused by the bacterium Salmonella enterica and is a global public health problem affecting millions annually.
- Clinical features include prolonged high fever, abdominal discomfort, diarrhea or constipation, and potential complications like intestinal perforation.
- Diagnosis involves blood, stool, or bone marrow cultures and serologic tests. Ceftriaxone is the treatment of choice for multidrug-resistant cases. Early diagnosis and appropriate antibiotic treatment are important to prevent complications.
Lecture FIVE -Filariasis Pathogenesis.pptobedcudjoe1
Lymphatic filariasis is caused by infection with Wuchereria bancrofti, Brugia malayi, or Brugia timori nematodes transmitted through mosquito bites. It manifests as lymphedema, elephantiasis, hydrocele, acute dermatolymphangioadenitis attacks, and tropical pulmonary eosinophilia. Over 1.2 billion people are at risk globally, with India accounting for over half of cases. Diagnosis involves blood smears, antigen tests, and clinical signs. Treatment focuses on mass drug administration to reduce transmission and managing symptoms through hygiene, antibiotics, and surgery.
Strongyloides stercoralis is a soil-transmitted helminth parasite with both free-living and parasitic life cycles. In its parasitic cycle, the filariform larvae penetrate the skin and travel to the lungs before migrating up the respiratory tract and into the small intestine where females reside. The females lay eggs which hatch into rhabditiform larvae that pass in the feces but can also develop into filariform larvae, allowing reinfection of the same host. Heavy infections can suppress the immune system and cause disseminated strongyloidiasis, a potentially fatal condition. Diagnosis involves finding larvae in stool or biopsy samples.
Enterobius vermicularis, commonly known as pinworms, are one of the most common intestinal nematodes. The adult worms inhabit the cecum and colon of humans. After mating, the male worms die while the female worms migrate out of the anus to lay eggs on the perianal skin, causing itching. Pinworms are transmitted through ingestion of eggs from contaminated surfaces or through autoinfection. Their lifecycle does not involve an intermediate or reservoir host. Diagnosis involves examining perianal skin for eggs using cellophane tape in the morning before washing. Treatment involves albendazole and repeated doses may be needed along with hygiene practices to prevent reinfection.
Hookworms are parasitic roundworms that infect the small intestine of humans. Two main species are Ancylostoma duodenale and Necator americanus. They penetrate the skin and migrate through the body before maturing in the intestine. Adults attach to the intestinal wall where they feed on blood, causing anemia. Symptoms include abdominal pain, fatigue, and impaired growth in children. Diagnosis involves finding hookworm eggs in feces. Treatment uses anthelmintic drugs like albendazole or mebendazole. Prevention focuses on improved sanitation and health education.
This presentation provides an overview of antibiotic-resistant gonorrhea for public health professionals. It defines antibiotic resistance and describes how gonorrhea has developed resistance to multiple antibiotic classes. It notes gonorrhea is the second most commonly reported infection in the US and resistance is present in 50% of cases. Untreated gonorrhea can lead to serious health issues and increase HIV risk. The role of public health leaders is outlined as detecting and preventing spread through infrastructure, following national strategies, promoting awareness and prevention services.
1. Mycobacteria are acid-fast, aerobic bacteria that include pathogens like Mycobacterium tuberculosis, M. leprae, and M. bovis. They are classified based on growth rate and pigmentation.
2. M. tuberculosis is the cause of tuberculosis and can infect the lungs and other organs. Atypical mycobacteria like M. kansasii can also cause pulmonary infections.
3. Laboratory diagnosis of tuberculosis involves microscopy, culture, and drug sensitivity testing of respiratory specimens. Leprosy is diagnosed by microscopy of skin and nerve tissue samples.
The document discusses the process of viral replication. It begins with an introduction that defines viral replication as the production of all viral components through an assembly process rather than cellular division. It then describes the 7 key steps in viral replication: 1) Attachment, 2) Penetration, 3) Uncoating, 4) Genome replication, 5) Assembly, 6) Maturation, and 7) Release. Each step is explained in more detail. The document concludes that viral replication follows common stages across all viruses but with differences imposed by the host cell and viral genome.
This document discusses various culture methods used to isolate and grow bacteria. It describes streak culture, lawn culture, stroke culture, stab culture, pour plate culture, and liquid culture. Streak culture is routinely used to isolate bacteria by streaking an inoculum across agar plates. Lawn culture provides uniform bacterial growth. Stroke and stab cultures are used to provide pure bacterial growth for diagnostic tests. Pour plate culture allows enumeration of bacterial counts. Liquid cultures are used for blood cultures and sterility tests. The document also discusses methods for establishing anaerobic conditions and various anaerobic media.
Viruses are intracellular pathogens that contain either DNA or RNA, surrounded by a protein capsid. Some viruses have an outer envelope. Viruses infect cells and use the cell's machinery to replicate their nucleic acid and make new viral particles. There are several shapes that viruses can take, including helical, polyhedral, and more complex shapes. Viruses are classified based on their nucleic acid, morphology, and replication strategy. Examples of viral families and the diseases they cause are provided.
This document discusses various methods used to identify unknown bacterial cultures, which is a major responsibility of microbiologists. It outlines staining techniques like Gram staining, acid-fast staining, endospore staining, and capsule staining. These techniques examine morphological characteristics of bacteria like shape, arrangement, presence of spores or capsules. The document also mentions biochemical tests that detect bacterial enzymatic activity or ability to ferment carbohydrates and produce acids/gases. Identifying pathogenic bacteria is important for medical diagnostics and food/brewing industries to prevent contamination.
The document summarizes microbiology techniques for culturing microbes and microscopy. It discusses the five steps for culturing microbes: inoculation, isolation, incubation, inspection, and identification. It then covers light microscopy and electron microscopy. Key points include how microbes are introduced to growth media, streak plating for isolation of pure cultures, observing colony morphology and gram staining under microscopes, and correlating results for identification. Microscopy techniques like brightfield, darkfield, phase contrast, and fluorescence are also outlined.
This document discusses the process of identifying infectious agents through culture and laboratory testing. It begins by defining key terms related to isolation, identification, and taxonomy of microbes. It then outlines the steps laboratories take to isolate microbes from samples via culture, identify them using staining and biochemical/genetic tests, and determine antibiotic susceptibility. Molecular techniques like PCR, sequencing, and protein/fatty acid profiling can also directly identify microbes or differentiate bacterial strains without requiring culture. The goal is to accurately identify the infectious agent to aid treatment and antibiotic selection.
How ti write a good scientific paper.pptobedcudjoe1
This document provides guidance on writing scientific papers. It discusses the typical structure of a journal paper, including sections like the abstract, introduction, methods, results, and discussion. It also provides 18 suggestions for writing good scientific papers, such as knowing your audience, using an outline to organize ideas, paying attention to grammar and tenses, and taking editorial comments seriously. The document emphasizes writing clearly and concisely for other scientists, with examples of how to effectively present and discuss results and cite references.
Strategies in writing JOURNAL ARTICLE.pptobedcudjoe1
The document provides guidance on writing and publishing journal articles. It discusses important considerations at various stages of the process, including choosing a suitable target journal, structuring the article, writing different sections, and submitting the article. Key sections covered include the introduction, literature review, methods, results, and discussion. The document emphasizes organizing the article in a clear and logical manner, using accurate and appropriate language, and addressing the journal's instructions for authors.
This document provides guidance on writing scientific papers. It discusses:
1. The key elements of a scientific paper including an introduction that provides context, a materials and methods section to allow reproducibility, presenting results clearly, and discussing findings and implications.
2. Structuring the paper with a reliable framework of addressing what, why, when, how, where and who.
3. Reasons for publishing including advancing scientific knowledge, career progression, and obtaining grants.
4. Tips for the writing process such as getting started, organizing, and responding to reviewer feedback.
This document provides guidance on writing and publishing scientific research papers. It discusses key aspects of research papers such as defining a clear research question, addressing only one main question per paper, and determining where to publish. The document outlines the typical structure of research papers, including the title, abstract, introduction, body, and conclusion. It also covers peer review processes and publishing ethics. Overall, the document serves as a guide for scientists on how to effectively write up and disseminate their research findings.
The document provides guidance on writing feature stories. It explains that feature stories tell a story using a beginning, middle, and end with liberal use of quotes and vivid descriptions. It recommends using a lead to grab the reader's attention, a nut graph to summarize the story, and a transition/quote formula to move between facts and quotes. It also provides examples of different types of leads and advice on ending the story powerfully by tying it back to the beginning.
This document provides tips for giving effective scientific presentations. It discusses including an introduction to build context, focusing each slide on one key concept or experiment, and using a structure that moves from general to specific details back to general. Presentation elements like font, font size, bolding, capitalization, spacing and references are covered. The conclusion restates that the document covered key points, structure and slide aesthetics to help give good presentations.
This particular slides consist of- what is hypotension,what are it's causes and it's effect on body, risk factors, symptoms,complications, diagnosis and role of physiotherapy in it.
This slide is very helpful for physiotherapy students and also for other medical and healthcare students.
Here is the summary of hypotension:
Hypotension, or low blood pressure, is when the pressure of blood circulating in the body is lower than normal or expected. It's only a problem if it negatively impacts the body and causes symptoms. Normal blood pressure is usually between 90/60 mmHg and 120/80 mmHg, but pressures below 90/60 are generally considered hypotensive.
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Here is a summary of Pneumothorax:
Pneumothorax, also known as a collapsed lung, is a condition that occurs when air leaks into the space between the lung and chest wall. This air buildup puts pressure on the lung, preventing it from expanding fully when you breathe. A pneumothorax can cause a complete or partial collapse of the lung.
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5. Classification of Strep from Humans
Species Lancefield Hemolytic Comments
S. pyogenes A β
S. agalactiae B β, γ Group B Strep
S. dysgalactiae
subsp. equisimilis
C, G β Formerly S. equisimilis;
pyogenic; respiratory, SSTI
S. pneumoniae None α
S. bovis species
group
D α, γ Viridans; associated with colon
cancer; IE
S. mutans group not useful α, γ, rarely β Viridans; dental caries and IE
S. salivarius group not useful α, γ Viridans; opportunistic
S. mitis group not useful α Viridans; IE, opportunistic
S. anginosus group A, C, F, G,
or no
detectable
α, β, γ Viridans; formerly known as S.
milleri; 3 species S. anginosus, S.
constellatus, and S. intermedius;
purulent infxns
6. Zoonotic Strep Species
Species Lancefield Hemolysis Comments
S. dysgalactiae
subsp dysgalactiae
C, L α, β, γ Domesticated animals
S. equi subsp equi C β Equine strangles; limited
documentation of human infxn
S. equi subsp
zooepidemicus
C β Bovine mastitis; outbreaks of human
nephritis
S. pornicus E, P, U, V β Swine; human female genital tract;
may cross react w/ GBS antigen
testing
S. canis G β Dogs; infrequent human pathogen
S. suis R, S, T α, β Swine; infrequent human meningitis
S. iniae None
detectable
β Fish; SSTI, sepsis
7. Case 1
• 12F
– Developed fevers, sore throat, swollen cervical lymph
nodes 3 days ago
– Several kids at school sick recently
– Today, developed an erythematous, blanching rash on
torso, a redness on face sparing area around lips, and a
coating on tongue.
– She’s allergic to PCN.
• Questions
– What clinical condition? What pathogen?
– How to diagnose? How to treat?
– What complications to worry about?
8. Streptococcus pyogenes
• Group A Strep, GAS; human-restricted pathogen
• Cell-associated virulence factors
– Hyaluronic acid capsule
• Antiphagocytic
• Not immunogenic
– M protein (over 150 types); other genes with similar proteins
• Antiphagocytic
• Bind IgG, IgA
• Iron transport
• Resistance to antimicrobial peptides
– Lipoteichoic acid (LTA)
• Extracellular products
– Streptolysin S (SLS): oxygen stabile
– Streptolysin O (SLO): oxygen labile
– DNases
– Streptokinase: dissolves clots
– SpeB (streptococcal pyogenic exotoxin): protease
– SpeA and SpeC: scarlatinal toxins associated with scarlet fever
– Superantigens
10. Antibiotic Options for GAS
• Try to use PCN or β-lactam if at all possible!
• Cephalosporins, carbapenems have great
activity
• Clinda generally active; sporadic resistance
• Increasing resistance to azithro, quinolones
• Common resistance to tetracycline family
• TMP/SMX questionable (assume inactive)
• Vanco, dapto, linezolid
11. Streptococcal Pharyngitis
• Ages 5-15 highest incidence; adults also infected (e.g., military
recruits)
– Person-to-person transmission via droplets or secretions; proximity
and crowding worsen!
– Food- and water-borne outbreaks occur
• Acute onset sore throat, fever, malaise, HA
– Look for GI sx in kids
– Enlarged, hypermic tonsils, exudates
– Tender cervical LAD
– Cough, coryza, conjunctivitis should suggest alternative dx.
• Self-limiting in about one week
– Treat to hasten resolution, stop spread, reduce sequelae
• Dx by cx or rapid antigen testing
• Oral PCN-V, IM PCN-G, oral amox; cephalexin, azithro, clinda
12. Strep Pharyngitis (con’t)
• Remember that 10% of kids asymptomatically
colonized (lower in adults)
• Cultures or rapid antigen test may remain positive after
tx; don’t retreat unless sx have recurred.
• Watch for suppurative complications: peritonsillar
abscess, retropharyngeal abscess, lymphadenitis,
mastoiditis, meningitis, brain abscess, thrombosis of
intracranial venous sinuses
13. Scarlet Fever
• Classically associated with pharyngitis, but may occur
after infxns at other sites
• Recent outbreak in China and Hong Kong
• Requires GAS strain with erythrogenic toxins
• Rash typically on 2nd day
– Face flushed except for circumoral pallor
– Enanthem: small, hemorrhagic spots on hard and soft
palate
– Exanthem: upper chest to torso, extremities; face, palms,
soles spared; diffuse blush with points of deeper red that
blanch; Pastia’s lines (skin folds deeper red)
– Tongue: coated to red strawberry tongue
15. Acute Rheumatic Fever (ARF)
• Non-suppurative inflammatory lesions of heart, joints,
subcutaneous tissues, CNS
• Follows an upper respiratory GAS infection
• Molecular mimicry?: Ig’s to M protein react with
cardiac myosin, synovium, and articular cartilage
• Occurs in 0.4 to 3% of untreated GAS pharyngitis cases
– More recent ECHO studies suggest rate may be 10x higher
than thought
• Worldwide: 500,000 ARF per year, with 300,000
developing rheumatic heart disease
• Recurrence rate higher with subsequent GAS infection
16. ARF
• Major manifestations
– Carditis: murmur, CHF, pericardial friction rubs or effusions; chronic mitral >
aortic valves
– Polyarthritis: knees, ankles, elbows, wrists
– Chorea: Syndenham’s chorea (St Vitus dance); emotional lability, weakness,
involuntary purposeless movements
– Subcutaneous nodules: firm, painless; few mm to 2cm
– Erythema marginatum: non-pruritic, non-painful eruption on trunk;
evanescent, serpiginous.
• Minor: fever, arthralgia, heart block, acute-phase reaction in blood labs
• 1-5 weeks after GAS infxn; avg 19 days. Lasts 3 months.
• Carditis in 40-50% first ARF, only sx posing long-term disability or death
• Dx using criteria above, plus evidence of GAS infection by either culture or
rising GAS antibody titer (ASO or DNaseB).
• Tx: depends on severity, analgesics to aspirin to steroids
19. ARF Treatment: Secondary Prevention
• Prevention of recurrence
– IM benzathine PCN-G q3-4 weeks
– Oral PCN-V or sulfasalazine 2nd line
– Erythro for allergic
– Duration depends on severity
Category Duration after last attack
RF w/o carditis 5 years or age 21 (whichever longer)
RF w/ carditis but no residual heart
(valvular) disease
10 years or age 21 (whichever
longer)
RF w/ carditis and residual heart
(valvular) disease
10 years or age 40 (whichever
longer); maybe lifelong
20. Poststreptococcal Acute
Glomerulonephritis
• GAS, but also group C (S. equi subsp
zooepidemicus); certain M-types and groups
associated
• Occurs after either pharyngitis or pyoderma; up
to 15% untreated cases
• Recurrences less frequent than with ARF
• Believed to be immunologic etiology: cross-
reaction vs. deposition of Ab-Ag complexes
• Worldwide: 470,000 cases/year, with 5000 deaths
21. PS-AGN
• S/Sx (10-21 days latent): HTN, edema, discolored urine;
malaise, HA, anorexia. Fever very uncommon.
– Facial, periorbital swelling common
– CHF-like respiratory sx
– Labs: anemia; ESR up; low serum protein; BUN, Cr up; total
complement and C3 down
– Urine: mild hematuria, mild proteinuria
• Dx: clinical hx, physical findings, evidence of recent Strep
infection; maybe bx
• Tx: fluid management; treat Strep (PCN); check contacts
• Secondary prophylaxis is unnecessary (b/c recurrences very
rare).
22. Case 2
• 39M, no pmhx
• Pulled calf exercising at gym 4 days ago, took ibuprofen
• 2 days later, developed pain, redness near site
• ED: low grade temp; erythema on calf, warm, traced; dx
cellulitis, started IV vanco.
• Overnight, redness expands, becomes more tender, spiking
fevers
• Noon: febrile, tachycardic, soft BP; erythema deeper, no
pain. WBC 15.
• Questions
– FIRST intervention?
– Change in treatments?
23. Necrotizing Fasciitis
• Erysipelas or cellulitis progresses from excessive pain to
loss of pain sensation, hemorrhagic bullae, rapidly
advancing border
• Commonly very ill
• Dx: need to think of it; pathologic dx
– Laboratory Risk Indicator for NF (LRINEC): combines WBC, Hgb,
CRP, Na, glucose, Cr
• Tx:
– Debridement (often multiple times)
– Antibiotics: PCN and clindamycin
• Consider toxic shock syndrome
• Remember: not all NF is GAS
24. Streptococcal Toxic Shock Syndrome
• Any Strep infxn with sudden onset of shock and organ
failure (most common with skin site)
• At least 11 toxins with superantigen activity, but likely
many factors contribute
– Activates 1 in 5 T cells (compare to 1 in 10,000 to 100,000
in normal infections) (Mueller-Alouf et al., 1994).
– Result is cytokine Armageddon
TNF-α, IL-1β,
IL-6, TNF-β,
IL-2, IFN-γ
25. Strep TSS
• Sx:
– Phase 1: fevers, chills, myalgias, GI sx, confusion, combative
– Phase 2: tachycardia, tachypnea, fevers
– Phase 3: shock and organ failure
– If skin focus, sx evolve at site
• Tx:
– Source control!
– ICU (ARDS in 55% cases)
– RRT (renal failure in 50% cases)
– Abx: PCN and clinda (high dose) (A-II rec)
• Vanco, dapto, linezolid, Synercid for PCN-allergic
– Maybe IVIg (B-II rec)
26. Why clinda?
• Protein synthesis inhibitor: shuts down toxin production
• PCN has Eagle effect: less active against stationary phase GAS
– May be due to change in PBP expression
– No such issue for clinda
• Clinda 600-900mg IV q8h
• Limited clinical data
– Zimbelman et al., 1999 (looked at NF)
27. So what about IVIg?
• IVIg: some Abs to GAS toxins; improve immune milieu
• Clinical data is incomplete
– Darenberg et al., 2003
• PCN (12 g/day), clindamycin (600 IV TID), +/- IVIG (1 g/kg day 1, 0.5
g/kg days 2 and 3)
• 10 IVIg, 11 placebo
• IVIg had trend towards decreased mortality at 28 days (p=0.3),
faster resolution of shock, faster improvement in end-organ
failure; slower resolution of NF
• No adverse events from IVIg.
• Cost: about $75-100/gram…so this study regimen
would add between $10,500 and $14,000 for 70kg
adult.
28. Case 3
• 23F IVDU admitted with septic arthritis
• No hx recurrent infxns as child
• Aspirated fluid shows GPC diplococci
• Blood cultures later grow same, α hemolytic
• Questions
– Antibiotic tx?
– Other testing?
29. Streptococcus pneumoniae
• Micro lab identifies by α hemolysis, catalase negative,
susceptible to Optochin, and dissolved by bile acids.
• Polysaccharide capsule: 91 serogroups and counting
• Naturally competent (can take up DNA)
• Doesn’t make highly toxic, tissue-damaging products
• Niche is human nasopharynx: 5-10% healthy adults and
20-40% healthy kids colonized
• Very young and very old most susceptible to invasive
disease, but epidemiology changing with vaccination.
30. Factors that Predispose to
Pneumococcal Disease
• Extremes of age
• Defective Ab formation
• HIV
• Complement defects
• Few or ineffective PMNs
(steroids, EtOH, DM)
• Asplenia (incl sickle cell)
• Excess exposure
(daycare, prison,
shelter)
• Prior respiratory infxn,
esp flu
• Pulmonary
inflammatory (smoking,
COPD)
31. Pneumococcal Pneumonia
• Often multiple risk factors
• Cough, fatigue, fever, chills, SOB
• Lung exam abnormal
• CXR: usually infiltrate; air bronchograms correlate with
bacteremia; frequent effusion, and rare empyema.
• Labs: leukocytosis, but rare leukopenia
• Dx: sputum cx +/- blood cx (can have neg sputum but
pos blood cx). Ag test positive in 80% of cases, 10%
w/o pneumococcus; can pick up colonization in kids so
don’t use in pediatrics.
• Complications: empyema; cardiac events
32. Other Clinical Syndromes of
Pneumococcus
• Otitis media
– Usually #1 or #2 to H. flu.
• Sinusitis
– Usually #1 or #2 to H. flu.
• Meningitis
– Most common bacterial meningitis in adults; also in kids >6 mos in countries w/ Hib vaccine
– Direct extension or bacteremia
• Exacerbation of chronic bronchitis
– 2nd to H. flu.
• Conjunctivitis
• Endocarditis (uncommon)
• Purulent pericarditis (rare)
• Septic arthritis
• Osteomyelitis (esp of vertebrae)
• SSTI
• If an uncommon pneumo infection in young person…check HIV.
33. Treating Pneumococcus
• In 2008, MIC breakpoints for pneumococcus differentiated CNS
from all other sites
• Came from observation that you can’t get PCN into CSF at high
concentrations, but good levels in lung and other sites.
• Also picking up genes for altered PBPs.
Antibiotic Susceptible Intermediate Resistant
PCN (oral) ≤0.06 0.12-1 ≥2
PCN (IV), non-CNS ≤2 4 ≥8
PCN (IV), CNS ≤0.06 n/a ≥0.12
Amox (oral), non-CNS ≤2 4 ≥8
CTX, non-CNS ≤1 2 ≥4
CTX, CNS ≤0.5 1 ≥2
35. Treatment Recommendations
• Otits media: amox; amox/clav, quinolone, or
CTX if fails
• Sinusitis: amox, amox/clav, quinolone…if truly
bacterial (see recent guidelines)
• PNA: quinolone, macrolide, doxy, amox +/-
clav for outpatient; PCN, amp, CTX, vanco,
quinolone; typically 7-8 days total.
• Meningitis: vanco plus CTX, plus steroids;
narrow abx when MICs known
36. Pneumococcal Vaccinations
• Two flavors of vaccine:
– Pneumovax: capsular polysaccharide of 23 serotypes; PPS23
– Prevnar: capsular polysaccharide conjugated to protein
(improves humoral response), 7 serotypes originally, now up to
13; PCV13
• Recommendations
– Use PCV13 for kids; multiple shot protocol
– Adults with immunocompromise, asplenia, etc…get one dose of
PCV13, then one PPS23 at least 8 weeks later, and 5 years
thereafter.
– Adults over 65: PPS23 once
• These guidelines change frequently!
37. Changes in Capsule Type after
Vaccination Introduced
• May have replacement in colonization types.
• Other countries found invasive diseases increasing
from non-vaccine strains.
• Herd protection.
Invasive pnuemo
infections in kids
<5. From CDC.
38. Streptococcus agalactiae (Group B
Streptococcus)
• Capsule is most significant virulence factor
• Colonizes genital and lower GI tracts of 10-
40% of women; also found in oropharynx,
upper GI
• Pass to baby peripartum by ascension or
during birth
39. Neonatal Infections
• Early-Onset
– 12 hours of age average
– Bacteremia (85%), pneumonia (10%), meningitis (5-10%)
– Heavy maternal carriage (untreated), delivery at less than
37 weeks, intra-partum fever, intra-amniotic infection,
ROM >18 hours
• Late-Onset
– Median 36 days (7-89)
– Bacteremia (65%) and meningitis (25-30%)
• Treatment involves ampicillin plus aminoglycoside
initially, before move to PCN-G
40. Infections in Adults
• Found with predisposing factors, incl DM, liver disease, malignancy, renal
failure
• Puerperal infection of mother
– Upper genital tract; amniotic fluid, bacteremia, endometritis
• Primary bacteremia
• Pneumonia
• Endocarditis
– Large, friable vegetations; rapid valve destructions
• Arthritis
• Osteomyelitis
• SSTI
• Recurrent GBS infection
– 4% of cases will have another invasive GBS infection
• Treat: PCN-G (or vanco); add gent for endocarditis
41. Prevention
• Screening pregnant women led to 65% drop in early-onset
GBS illness in newborns.
– Lower vaginal and rectal swab at 35-37 weeks (unless going to
treat already b/c of hx)
• Intrapartum abx for:
– Positive screening
– Previous infant w/ invasive GBS
– GBS bacteriuria during current pregnancy
– GBS status unknown, plus delivery <37 weeks or ROM >18 hours
or fever
• No intrapartum abx for planned C-section in absence of
labor or membrane rupture.
• PCN; cefazolin or vanco for allergies
42. Case 4
• 67M with HTN, DM, COPD, CAD admitted w
cough, SOB, LE edema; afebrile; CXR fluid vs
multifocal PNA
• Given dose of levoflox in ED
• One blood cx drawn at admit: GPC pairs and
chains Strep viridans
• Questions:
– How do we interpret the blood cx?
43. Strep viridans
• Made up of 5 groups
– anginosus group
– mitis group
– mutans group
– salivarius group
– sanguinis group
• Normal flora of animals and humans
• Low virulence; no toxins
44. Strep viridans: Endocarditis
• Often with previous valvular pathology
• Proportion increases with time after valve
replacement
• Subacute: often weeks
• Fever, malaise, anorexia
• Low-grade bacteremia (1-30 CFU per mL blood)
45. Treatment of Native Valve Endocarditis
from Strep viridans and Others
Organism Antibiotic Regimen
PCN-sens Strep viridans (MIC ≤0.12) PCN-G (12-18 million U daily, divided) or CTX
(2g q24h) x 4 weeks
PCN-G or CTX plus gentamicin (3 mg/kg
qday) x 2 weeks
Vancomycin x 4 weeks
PCN-intermed Strep viridans (>0.12
but ≤0.5)
PCN-G (24 million U) or CTX (4 weeks) plus
gentamicin (2 weeks)
Vancomycin x 4 weeks
PCN-resistant Strep viridans (>0.5),
Abiotrophia, Granulicatella, Gemella
PCN (18-30 million U) or amp (12g/day,
divided) plus gentamicin x 4-6 weeks
Vancomycin x 6 weeks
At BMC in 2011, 20% of Strep viridans were intermediate MIC vs.
80% sensitive.
46. Treatment of Prosthetic Valve IE with
Strep viridans
Organism Regimen
PCN-susceptible (MIC ≤0.12) PCN-G (24 million U) or CTX (2g q24h)
x 6 weeks +/- gentamicin (3 mg/kg
q24) x 2 weeks
Vancomycin x 6 weeks
PCN-resistant (MIC>0.12) PCN-G (24 million U) or CTX (2g q24h)
plus gentamicin x 6 weeks
Vancomycin x 6 weeks
47. Other Manifestations of Strep viridans
• Bacteremia
– Account for 2.6% of all positive blood cultures
– After toothbrushing, 25-50% of people have bacteremia
– If transient, may consider limited clinical significance.
– More common and profound in ONC patients, esp BMT.
Bad outcomes (maybe just marker of bad mucosal
barriers?)
• Meningitis
– Rare: 0.3 to 5% of culture-positive meningitis
– However, concern about contamination
• Pneumonia
– Very rarely the sole, instigating pathogen
48. IE Prophylaxis: IDSA Guidelines
• “bacteremia resulting from daily activities is much more likely to cause IE than
bacteremia associated with dental procedures”
• Only people with certain conditions get ppx:
– Prosthetic valves or perivalvular material
– Previous IE
– Congenital heard disease, only cyanotic CHD, repaired CHD with prosthetic materials within
last 6 mos, repaired CHD with defect
– Cardiac transplant w/ cardiac valvulopathy
• Procedures warranting ppx:
– Dental procedures manipulating gingiva or cutting mucosa
– Respiratory tract
– Infected skin, skin structures, or musculoskeletal tissue
– NOT needed for GI or GU procedures, vaginal delivery, hysterectomy, tattooing.
• Regimens
– Amoxicillin 2g PO x 1, 30-60 min before procedure
– Keflex (2g), clinda (600mg) or azithro (500mg) PO x 1
49. Streptococcus anginosus group
• Formerly called Strep milleri group
• S. intermedius, S. constellatus, S. anginosus
• Viridans strep, but cause pyogenic infections
• Caramel-like odor of colonies
• Commensals of oropharyngeal, urogenital, and GI
• Synergize with other bacteria, esp anaerobes
• More toxins than other viridans
• Clinical conditions
– Dental abscess, CNS abscess, liver abscess, empyema
– IE: high myocardial abscess, metastatic abscesses
• Sensitive to PCN, CTX generally; vanco, clinda for allergy;
resistant to AG’s although still synergy; macrolides poor
50. Streptococcus dysgalactiae subsp
equisimilis
• Group C or G by Lancefield; had several older species rolled into it.
• Common flora of oropharynx, skin
• Infxns often mimic GAS or GBS infections
– Pharyngitis
• Get ASO bump
• PS-AGN has been documented, but not ARF
– SSTI
• Pyoderma, erysipelas, impetigo
• May be more common cause of cellulitis than GAS
– Arthritis, often polyarticular
– Osteomyelitis
– Endocarditis: acute to subacute; poor response to β-lactam monotherapy;
frequent emboli
• Tx
– PCN; amox, vanco, linezolid, cefazolin
– Naf, ox not effective; high rates of tetra, clinda, ery resistance
– Very good synergy b/w PCN and gent
51. Streptococcus bovis group
• Complex phylogeny, but S. gallolyticus subsp
gallolyticus is one associated w/ IE and bacteremia
• Causes 11-27% of all IE, and 24% Streptococcal IE
• High association with colonic malignancy and
hepatobilliary disease (77% of bacteremias found to
have CA in one series)
• Aortic valve most common
• Follows Strep viridans treatment guidelines
• Rare vancomycin resistance (probably acquired from
VRE)
52. Nutritionally Variant (Deficient) Strep:
Abiotrophia and Granulicatella
• Originally called Streptococcus mitior
• Require pyridoxal or cysteine for growth
• Small colonies; often satellites around other species; somewhat
difficult to culture
• Normal flora of upper respiratory, GI, UG tracts
• In vitro MICs don’t correlate well with clinical responses
– Less susceptible to PCN (33-67% relatively resistant)
– Vancomycin active
– PCN or vanco have synergy with gentamicin
– Decr susceptibility to 3rd gen cephs, azithro, clinda
• Cause IE (esp Abiotrophia): 5% of bacterial IE, majority of culture-
negative IE (although cultures more sens now)
– Compared to other bacterial IE: more complications, more
embolization, more CHF, more surgery needed, more relapses despite
appropriate tx
53. Streptococcus iniae
• β hemolytic; no Lancefield antigen
• May be misidentified as a viridans by
automated systems
• Cellulitis of hand(s) with accompanying
bacteremia
• Handling live or dead fish (especially tilapia)
• Good response to β-lactam abx
54. Case 5
• 49M admitted 2 week ago with ICH,
complicated ICU post-op course incl MRSA
VAP, today day 5 of 7 vancomycin
• Fever today, tachycardic; WBC up
• Blood cx drawn from CVC growing GPC pairs
and short chains
• Questions:
– What organism(s) do you worry about?
– What is your next step?
55. Enterococcus
• Part of Streptococcus until 1984.
• Can grow in 6.5% NaCl and from 10°-45°C;
hydrolyze esculin in presence of 40% bile salts
• Most infections from E. faecalis or E. faecium;
leading cause of nosocomial infxns
• Colonize GI tract; selected for by abx
56. Enterococcus: Clinical Manifestations
• Bacteremia +/- IE (1-32%)
– Frequent comorbidities
– IE subacute; fever, constitutional sx; 50% CHF; emboli 27-43%;
death 11-35%
• UTI
• Meningitis
– 0.3 to 4% of cases; usu severe comorbidities
• Abd Infxn
– Unclear contribution to pathology in polymicrobial collections
– Nosocomial peritonitis, PD-related infxn
• Neonatal
• SSTI
57. Enterococci: Challenges of Treatment
• Intrinsically resistant to many abx, with
acquisition of additional resistance
• Looking for bactericidal tx for IE
• β-lactams not regularly bactericidal as
monotherapy, requiring AG as synergy
58. β-lactams and Enterococci
• MICs 10-100x higher than Streptococci; ampicillin retains
highest potency, followed by PCN-G and carbapenems.
• E. faecium is usually resistant
– Overexpress pbp5, decreasing affinity
• E. faecalis rarely resistant, but may express a β-lactamase
(not readily detected without specific testing)
– For faecaLis, β-Lactams still work.
• Ceftaroline has good in vitro activity against E. faecalis (but
not amp-resistant E. faecium).
• Ceftriaxone or cefotaxime in combination with high-dose
ampicillin for E. faecalis IE with resistance to AGs
59. Vancomycin
• Resistance develops through acquisition of
genes that alter cell wall biochemistry
– VanA most common; VanB, VanC also clinically
found
– Changes D-ala-D-ala to D-ala-D-lactate, leading to
1000-fold decrease in affinity
• Televancin not very active against VRE
60. Other Drugs
• Daptomycin
– May want to use higher dose, 8-10 mg/kg
– Resistance rare
• Linezolid
– Resistance may be increasing
• Tigecycline
– Appears active against both VSE and VRE
• Synercid (quinupristin/dalfopristin)
– Not active against E. faecalis
• Quinolones
– Sometimes used in combination regimen for salvage
• Chloramphenicol
61. BMC Enterococcus Sensitivity Patterns
Drug All Enterococcus E. faecalis* E. faecium*
Ampicillin 68% 96% 7%
Gent (synergy) 78% 71% 100%
Levoflox 52% 60% 0%
Linezolid 100% 100% 100%
Nitrofurantoin 67% 100% 0%
PCN 63% 83% 0%
Synercid 34% 0% 100%
Streptomycin
(synergy)
73% 53% 83%
Tetracycline 19% 30% 14%
Vancomycin 71% 77% 0%
* Only speciated for certain cultures, like blood.
62. Treatment Guidelines for Enterococcal
IE
Resistance Pattern
PCN AG Vanco Regimen
S S S Amp or PCN plus AG x 4-6 weeks
(? Amp plus CTX if lose AG)
Vanco plus AG x 6 weeks
R S S Amp/sulbact + AG x 6 weeks (only if β-
lactamase producer)
Vanco plus AG x 6 weeks
AG: use gent if sensitive; consider streptomycin if sensitive.
64. Leuconostoc species
• Catalase-negative, GPCs pairs or chains; plants and
dairy products; rare opportunistic pathogens
• Intrinsically resistant to vancomycin
• Bacteremia, IE, pulmonary infections, meningitis, brain
and liver abscesses
• Must get MICs
• Usually sensitive to PCN and Amp, although MIC’s
usually higher than for Strep
• Dapto, carbapenems have good activity
• Poor activity of trimethoprim, sulfonamide, fosfomycin
65. Ongoing Areas of Research
• GAS
– Vaccine?
– Linezolid instead of clinda?
– Mechanisms of persistence and recurrence
– Genetic plasticity and evolution of new strains
• Pneumococcus
– Serotype replacement?
– Non-capsule vaccine?
• GBS
– Vaccine?
• Enterococcus
– Management of MDR
66. Where to Look for Help?
• www.idsociety.org
– IDSA website
– Practice guidelines for SSTI, IE