HSV Infections
Asymptomatic, mucocutaneous, neonatal, CNS, latent
Type 1: gingivostomatitis, whitlow, keratoconjunctivitis, encephalitis, eczema
herpeticum
Type 2: genital HSV, meningitis
Classification: primary; non primary, first episode; recurrent, reinfection Latency: sensory or autonomic neurons; LATS Reactivations: trauma, sunlight, stress (despite antibodies) Host: normal vs. immunocompromised
Neonatal HSV Infections
Congenital 5%; most HSV 2 (poorer prognosis)
Most mothers asymptomatic; antibodies may modify
Attack rate after primary maternal infection over 50% (> 10 times
than after recurrent infection) Cesarean section controversial in women with recurrent HSV at delivery Culture baby (eye, skin, throat) after 24 hours old Categories, prognosis: skin/eye/mouth, CNS, disseminated Symptoms: skin vesicles, fever, intractable seizures, pneumonia, DIC, conjunctivitis, recurrent skin vesicles after therapy
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Showing posts with label infections. Show all posts
Showing posts with label infections. Show all posts
Sunday, April 5, 2009
Cardiac Infections
Infective endocarditis. Streptococci and Staphylococci make up a very large fraction of cases of infective endocarditis, with Streptococci accounting for 50 to 60% of such infections and Staphylococci accounting for another
25%.
The viridans group of Streptococci includes the nutritionally variant organism which now has a new genus. They are now called abiotrophia. Abiotrophia defectivus. These are organisms that look like a viridans or any green hemolytic Streptococci that have unusual nutritional requirements.
Enterococci. Enterococcal infections are much less common in kids then they are in adults, and it is certainly true for endocarditis.
Occasionally, we have seen other Streptococcal organisms. Strep pneumoniae in beta hemolytic Streptococci, such as group C and T, Bs occasionally. So, this is the predominant group of origin. The two situations in which Staphylococci are particularly common, as far as this hemolytic carditis, are in the postoperative patient and in the patient who developed endocarditis in a normal heart.
The other common group of endocarditis agents that must be mentioned are the HACEK group. They account for 5 to 10% of cases of endocarditis.
About 5 % of cases of endocarditis are caused by other agents. Fungi, particularly Candida.
Aerobic gram negatives are not common in endocarditis, except occasionally in line-associated infections and in IV drug abusers; 3 to 5% of endocarditis is culture negative endocarditis and we will talk a little bit about that later on.
Pathogenesis of this disease. There is turbulent blood flow. In pediatric
lesions very often there is a jet effect, and in addition to the jet effect there is also non linear blood flow and eddies of blood. As a consequence of the jet effect, there is often endothelial disruption that occurs, which cumulates the development of the sterile fibrin-platelet thrombus in this area of endothelial damage or disruption. This is an outstanding place for "stray bacteremia" to settle out of the few organisms that become entrapped in this sterile fibrin-platelet fibrin. The slower the blood flow, the greater the opportunity for such organisms to be entrapped.
There are two presentations of infective endocarditis. The patient who
presents acutely is very sick with high fever and very toxic. They may be in congestive failure, and this is the situation where most often one would expect to find Staph aureus as the etiologic agent of the endocarditis. Situations where this presentation is most common is in a patient in the early postoperative phase, who has recently had heart surgery and had lines in place, or the unusual patient who presents with endocarditis with a normal heart without any obvious antecedent event. Other patients who are not postoperative but who have indwelling lines may also become infected with Staph aureus.
The other rather distinctive presentation, and more common presentation of endocarditis, is a much more insidious one. Patients may have low-grade fever or no fever, they are non-toxic. They do not feel very well, they have malaise, decreased energy. These infections are most commonly due to the viridans Streptococci. The HACEK group and fungi also produce infections that are more insidious and subacute in their presentations. Of course, we have patients who do not quite fit exactly in this category.
.... CLICK HERE TO DOWNLOAD FULL ARTICLE
25%.
The viridans group of Streptococci includes the nutritionally variant organism which now has a new genus. They are now called abiotrophia. Abiotrophia defectivus. These are organisms that look like a viridans or any green hemolytic Streptococci that have unusual nutritional requirements.
Enterococci. Enterococcal infections are much less common in kids then they are in adults, and it is certainly true for endocarditis.
Occasionally, we have seen other Streptococcal organisms. Strep pneumoniae in beta hemolytic Streptococci, such as group C and T, Bs occasionally. So, this is the predominant group of origin. The two situations in which Staphylococci are particularly common, as far as this hemolytic carditis, are in the postoperative patient and in the patient who developed endocarditis in a normal heart.
The other common group of endocarditis agents that must be mentioned are the HACEK group. They account for 5 to 10% of cases of endocarditis.
About 5 % of cases of endocarditis are caused by other agents. Fungi, particularly Candida.
Aerobic gram negatives are not common in endocarditis, except occasionally in line-associated infections and in IV drug abusers; 3 to 5% of endocarditis is culture negative endocarditis and we will talk a little bit about that later on.
Pathogenesis of this disease. There is turbulent blood flow. In pediatric
lesions very often there is a jet effect, and in addition to the jet effect there is also non linear blood flow and eddies of blood. As a consequence of the jet effect, there is often endothelial disruption that occurs, which cumulates the development of the sterile fibrin-platelet thrombus in this area of endothelial damage or disruption. This is an outstanding place for "stray bacteremia" to settle out of the few organisms that become entrapped in this sterile fibrin-platelet fibrin. The slower the blood flow, the greater the opportunity for such organisms to be entrapped.
There are two presentations of infective endocarditis. The patient who
presents acutely is very sick with high fever and very toxic. They may be in congestive failure, and this is the situation where most often one would expect to find Staph aureus as the etiologic agent of the endocarditis. Situations where this presentation is most common is in a patient in the early postoperative phase, who has recently had heart surgery and had lines in place, or the unusual patient who presents with endocarditis with a normal heart without any obvious antecedent event. Other patients who are not postoperative but who have indwelling lines may also become infected with Staph aureus.
The other rather distinctive presentation, and more common presentation of endocarditis, is a much more insidious one. Patients may have low-grade fever or no fever, they are non-toxic. They do not feel very well, they have malaise, decreased energy. These infections are most commonly due to the viridans Streptococci. The HACEK group and fungi also produce infections that are more insidious and subacute in their presentations. Of course, we have patients who do not quite fit exactly in this category.
.... CLICK HERE TO DOWNLOAD FULL ARTICLE
Bone and Joint Infections
There are three different routes of infection in children. The most common seems to be the hematogenesis route, which gains entry into the bone from the blood stream. Less commonly is by direct inoculation and this can be a puncture wound, such as stepping on a nail or something. This can also occur following trauma or surgery. Finally, a particular spread, which is really rare in children and seems to be more common in adults with various disabilities, especially alterations in blood flow.
What is thought to happen from the hematogenesis standpoint is that the during a course of bacteremia, as the organisms enter into the bone through the nutrient artery towards the growth plate, there are these loose capillaries that are said to have sluggish blood flow in them. It is also thought that maybe there is a fully developed reticulum within this system. There does seem to be evidence of low oxygen within the metaphysis, and we always hear about this preceding history of trauma as a possibly predisposing factor. Perhaps this is simply disruptive blood flow, but the history of trauma to children is common, and it is hard to know what really this is contributing to the pathogenesis.
The nutrient artery penetrates into the diaphysis of the bone, moving up into the metaphysis and making a hairpin turn at the epiphysis. This is why it is in a long individual, at least for the tubular long bones, that osteomyelitis is more common at the ends of the bones because of these here hairpin turns.
More recently there is some evidence in animals, specifically chickens, who actually can develop osteomyelitis spontaneously. A chicken strain of Staphylococcus aureus that appears at the endothelium within the capillaries of bones have gaps, and it looks as if the organisms can actually access the capillary system to these particular gaps. If you take a Staph aureus and inject it into the blood of the chicken, within 12 hours you can see bacteria in some of these capillaries, and subsequently a day or two later, evidence of infection at the metaphyseal epiphyseal junction. So this is sort of an interesting animal experiment, perhaps showing that these epithelial gaps, at least in chickens, play some role.
Another factor in the development of osteomyelitis, at least relating to Staphylococcus aureus, is the organism that produces this sort of slimy stuff seems to make it more adherent to various portions of the bones and thus more commonly associated with osteomyelitis than those other organs.
Microbial etiology of osteomyelitis. In the neonate, the organisms most commonly associated with osteomyelitis are typically Group B streptococcus and Staphylococcus aureus. Very small babies may involve for various gram negative bacteria and certainly cause osteomyelitis as well as some other bacteria. In the infant and older child, Staphylococcus aureus is the most common cause. Streptococcus is the second most common.
Highly encapsulated organisms are unusual causes of osteomyelitis, but 3 to 5% of patients with acute osteomyelitis will have pneumococcus as the etiology.
In the older child, the same types of organisms are seen. Salmonella is an important pathogen in patients with sickle cell anemia.
With penetrating injuries, organisms associated with the soil or the skin or on clothes can of course lead to infection. Some of these injuries, such as injuries associated with lawn mower trauma, can grind the soil-type organism into the skin and ultimately into the bone.
Now, sacroiliitis is not necessarily specifically an osteo, it is an osteo-like illness we must keep in mind, especially in dealing with certain populations, especially those who are likely to ingest under pasteurized or nonpasteurized dairy products.
.... CLICK HERE TO DOWNLOAD FULL ARTICLE
What is thought to happen from the hematogenesis standpoint is that the during a course of bacteremia, as the organisms enter into the bone through the nutrient artery towards the growth plate, there are these loose capillaries that are said to have sluggish blood flow in them. It is also thought that maybe there is a fully developed reticulum within this system. There does seem to be evidence of low oxygen within the metaphysis, and we always hear about this preceding history of trauma as a possibly predisposing factor. Perhaps this is simply disruptive blood flow, but the history of trauma to children is common, and it is hard to know what really this is contributing to the pathogenesis.
The nutrient artery penetrates into the diaphysis of the bone, moving up into the metaphysis and making a hairpin turn at the epiphysis. This is why it is in a long individual, at least for the tubular long bones, that osteomyelitis is more common at the ends of the bones because of these here hairpin turns.
More recently there is some evidence in animals, specifically chickens, who actually can develop osteomyelitis spontaneously. A chicken strain of Staphylococcus aureus that appears at the endothelium within the capillaries of bones have gaps, and it looks as if the organisms can actually access the capillary system to these particular gaps. If you take a Staph aureus and inject it into the blood of the chicken, within 12 hours you can see bacteria in some of these capillaries, and subsequently a day or two later, evidence of infection at the metaphyseal epiphyseal junction. So this is sort of an interesting animal experiment, perhaps showing that these epithelial gaps, at least in chickens, play some role.
Another factor in the development of osteomyelitis, at least relating to Staphylococcus aureus, is the organism that produces this sort of slimy stuff seems to make it more adherent to various portions of the bones and thus more commonly associated with osteomyelitis than those other organs.
Microbial etiology of osteomyelitis. In the neonate, the organisms most commonly associated with osteomyelitis are typically Group B streptococcus and Staphylococcus aureus. Very small babies may involve for various gram negative bacteria and certainly cause osteomyelitis as well as some other bacteria. In the infant and older child, Staphylococcus aureus is the most common cause. Streptococcus is the second most common.
Highly encapsulated organisms are unusual causes of osteomyelitis, but 3 to 5% of patients with acute osteomyelitis will have pneumococcus as the etiology.
In the older child, the same types of organisms are seen. Salmonella is an important pathogen in patients with sickle cell anemia.
With penetrating injuries, organisms associated with the soil or the skin or on clothes can of course lead to infection. Some of these injuries, such as injuries associated with lawn mower trauma, can grind the soil-type organism into the skin and ultimately into the bone.
Now, sacroiliitis is not necessarily specifically an osteo, it is an osteo-like illness we must keep in mind, especially in dealing with certain populations, especially those who are likely to ingest under pasteurized or nonpasteurized dairy products.
.... CLICK HERE TO DOWNLOAD FULL ARTICLE
Saturday, April 4, 2009
Antibiotics and Outpatient Infections.pdf
When you are choosing an agent to use, you are looking at what clinical symptoms the patient has, who is this patient, an immunocompromised or normal host. You are taking a little bit more of a detailed history to include infectious risks, and you are thinking about the antibiotic itself.
In a clinical syndrome, you are trying to identify what is the predominant symptom and signs. You are trying to see where the site of infection is. Is this infection in the joint? Is this infection in the bone? Where are we treating this infection? Does this patient have a central nervous system infection? Then, identify the disease process because if you identify that this is osteomyelitis, it is a little bit different than if you think that the patient has pyogenic arthritis. The causative organisms might change and then what you need do, is you need to think of what the disease is, what are the most likely pathogens associated with this disease and what is their susceptibility pattern in the area where you practice. This is essential. To pick a drug, you have to know what organism you are dealing with. Because if not, you are really doing it blindly. So you have to have an idea of what organisms cause what specific diseases so that then you can make a good choice about antibiotic therapy.
When you look at hosts, you need to know the age of the patient. A 10-year-old is different from a neonate. The pathogens are different. Think about underlying conditions. Is this a patient with cystic fibrosis with pneumonia, or is this a well child with pneumonia? Different pathogens. So you are thinking about that host. Does this patient have an indwelling catheter? Does the patient have a prosthetic heart valve? All these things make it a little different to know which antibiotic to choose. Then, is the patient malnourished because that might be a cause for immunodeficiency.
When you are looking at a focused history, you need to know if the patient you are seeing with fever for 10 days has just come back from a safari in Africa, or is this a patient who has just been in the community where there is a lot of influenza. So you are going to ask about travel, about exposure to people who have contagious diseases such as tuberculosis, or whether the child is exposed to more infections because he is in daycare. Are immunizations up to date? That is very important. That patient may have measles if they have never been immunized and there is an increase in your community of Hemophilus influenza type E,. which is now very rare but can occur. Is this adolescent an IV drug abuser? Unfortunately, this happens occasionally and it brings in another set of organisms and diseases we have to think about, and then sexual activity brings up another whole host of organisms and disease processes.
.... CLICK HERE TO DOWNLOAD FUL ARTICLE
In a clinical syndrome, you are trying to identify what is the predominant symptom and signs. You are trying to see where the site of infection is. Is this infection in the joint? Is this infection in the bone? Where are we treating this infection? Does this patient have a central nervous system infection? Then, identify the disease process because if you identify that this is osteomyelitis, it is a little bit different than if you think that the patient has pyogenic arthritis. The causative organisms might change and then what you need do, is you need to think of what the disease is, what are the most likely pathogens associated with this disease and what is their susceptibility pattern in the area where you practice. This is essential. To pick a drug, you have to know what organism you are dealing with. Because if not, you are really doing it blindly. So you have to have an idea of what organisms cause what specific diseases so that then you can make a good choice about antibiotic therapy.
When you look at hosts, you need to know the age of the patient. A 10-year-old is different from a neonate. The pathogens are different. Think about underlying conditions. Is this a patient with cystic fibrosis with pneumonia, or is this a well child with pneumonia? Different pathogens. So you are thinking about that host. Does this patient have an indwelling catheter? Does the patient have a prosthetic heart valve? All these things make it a little different to know which antibiotic to choose. Then, is the patient malnourished because that might be a cause for immunodeficiency.
When you are looking at a focused history, you need to know if the patient you are seeing with fever for 10 days has just come back from a safari in Africa, or is this a patient who has just been in the community where there is a lot of influenza. So you are going to ask about travel, about exposure to people who have contagious diseases such as tuberculosis, or whether the child is exposed to more infections because he is in daycare. Are immunizations up to date? That is very important. That patient may have measles if they have never been immunized and there is an increase in your community of Hemophilus influenza type E,. which is now very rare but can occur. Is this adolescent an IV drug abuser? Unfortunately, this happens occasionally and it brings in another set of organisms and diseases we have to think about, and then sexual activity brings up another whole host of organisms and disease processes.
.... CLICK HERE TO DOWNLOAD FUL ARTICLE
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