Diseases information. Disorders. Treatment. » Kawasaki Syndrome

Now coxsackie A-9

Jammy B. — Tue, 15 Apr 2008 15:36:54 +0000

Now coxsackie A-9; the reason I’m showing this is that this can cause rashes, maculopapular and petechial rashes, but it can also have vesicular and urticarial lesions. These frequently get misdiagnosed as contact dermatitis or poison ivy and bug bites. So this is a child who happens to have coxsackie A-9, has lesions that were quite pruritic and they look like papular urticaria. They look like bug bites. Urticaria around a central vesicular lesion. This is another enterovirus that looks like bug bites on this child, and this child as well. Also urticaria, large urticaria. This occurs in outbreaks that the first thing a lot of people think of are foods, but if you have this with fever it’s likely a viral infection, and it can be several different viruses, but particularly in the summertime, enteroviruses. This is a child that looks a little bit like having chicken pox but went on to have lesions that look like those you see in allergic purpura, and went on to have massive purpura that you see here. Looking like DIC, although she was not that sick. This for comparison is a child with scabies. If you scrape these lesions, if you scrape these other lesions you get nothing. You just get some normal epithelial cells if you do it vigorously. Whereas if you scrape poison ivy or if you scrape bug bites they are loaded with eosinophils. Here you can see the organism as well.
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The last of these is hand-foot-and-mouth syndrome, and this is the most distinctive enanthem/exanthem complex. The main etiology is coxsackie A-16 but this has been seen with other enteroviruses but in outbreak circumstances it has mainly been A-16. Or when it’s described to other viruses, they don’t usually have the complete syndrome. Most recently in Hong Kong and Taiwan they had an outbreak with enterovirus 71 and they described cases of hand-foot-and-mouth. The lesions most common on hands and then the feet and buttocks. The peripheral distribution is distinct and occasionally they will go away and then come back. So you will have recurring lesions and sometimes they’ll be chronic with immune defects and sometimes with no apparent immune defects. Chronic reoccurring lesions. This is a classic case of the lesions on the heel of this child and also the buttock. The buttock lesions are usually just maculopapular and not vesicles. This is the tongue of this child’s aunt, which looks like aphthous stomatitis and this is the grandmother of that child with typical lesions on the hands. This is just to show the size of the lesions. The other day I showed you Herpes simplex lesions on the soft palate, and this is almost a 2 cm lesion in the mouth of this particular child.
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Now I’m going to move on to roseola. Roseola and phantom exanthem subitum is a classic pediatric exanthem and about somewhere between 10-30% of children have roseola. It usually will occur in the first two years of life and the illness is fever for 3-5 days. The fever usually falls rapidly and then you have the appearance of the rash. But a lot of physicians just call the first rash they see in a child roseola, which you shouldn’t do. The illness is not seasonal but there have been occasional outbreaks. It has been associated with many different viruses, but recently, relatively recently, herpes virus 6 has been found to be the major cause of this but it’s not the only cause. The Japanese papers on this, the way they did their studies, it was destined to prove this was the cause. So the actual fact is there are multiple etiologies. It seems that this complex of fever and then fever dropping and rash occurring is a host phenomenon relating to multiple different virus antigens, of which the most important is probably herpesvirus 6.
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This is just an example of an outbreak of roseola that occurred in Rochester New York in 1974. This is the outbreak and from a number of these they isolated echovirus 16. So showing you that, at least in outbreak circumstances, enteroviruses may play a role.

Next is toxic shock syndrome

Jammy B. — Thu, 10 Apr 2008 14:15:44 +0000

Next is toxic shock syndrome and this is also a staphylococcal toxin and sometimes a streptococcal toxin. This is similar to the erythrogenic toxin of scarlet fever and very different from exfoliative toxin from phage group II staph. Here the classic disease of course was the epidemic relating to the staphylococcal infections with tampons, which the primary source went unrecognized and the manifestations were the toxic shock. It was actually described first in young children by Jim Todd relating to localized infections with disseminated toxin, usually skin infections. The manifestations; hypotension, clinical or laboratory abnormalities in greater than or equal to three organ systems, and reasonable evidence of ruling out other etiologies. This is desquamation in an adult with toxic shock. This is the sunburn-like rash and this is showing some generalized erythema and conjunctivitis. Just to go back to toxic shock; we occasionally see cases in, for example, group A streptococcal infections with pneumonia. You need to be aware of this. There is evidence now that treating these patients with IVIG benefits, decreases their degree of fever and their morbidity. Canadian drugs online
Okay, the last of the diseases that have some similarity with scarlet fever is erythema infectiosum and this is caused by parvovirus B19. It has a case-to-case interval of 6-14 days. The important thing is that after exposure about a week later you are contagious, but generally asymptomatic or have a mild fever. Then a week after that the rash occurs and at that time the patient is no longer contagious. The rash starts on the face with a “slapped cheek” appearance. The original rash starts centrally, spreads peripherally, is not very diagnostic, but takes on a lace-like pattern. The rash is more prominent on extensive surfaces and adults have arthralgias and arthritis. This is a classic picture from almost 100 years ago, showing the slapped cheek appearance with circumoral pallor. This is a little boy with a real disease. Not too unhappy. This is a picture of a lace-like rash and here is a photograph of what it looks like. The big issue of parvovirus B19 we’ve already mentioned as far as infection in pregnant women.
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Now I want to switch over and talk a bit about enteroviruses, and I’m going to say more at the end about enteroviruses. But a lot of clinical manifestations can occur with enterovirus infections. This is … almost 40 years ago I occupied my time studying these things so everybody yawns when I try to make a big deal out of this. So I’m just going to go through and give you some major manifestations of what you should be aware of. Then we’ll come back and talk specifically about enterovirus epidemiology. I’m going to talk about EcHO-9 coxsackie A-9 and coxsackie A-16 as examples. EcHO virus 9 was the first of the enteroviruses to be well characterized with exanthems, with exanthem and aseptic meningitis. That you have fever, headache, nuchal rigidity, nausea, vomiting, various findings relating to aseptic meningitis. Rash occurs in about one-third of the cases but it’s adversely related to age. The older you are, the less likely you are to have rash. Other findings are typical enterovirus manifestations. The rash is rubelliform, erythematous, maculopapular, discreet. Generally starts centrally. It looks like this, and there are also some petechiae here. This is another child with petechial lesions. So the important thing here is that you have an illness with fever, some evidence of meningitis and on LP they have aseptic meningitis. The cell count usually in the meningitis has a predominance of polys early and you have petechiae popping out right in front of you as well as a rash. So the big thing is differential from meningococcemia. And this you can’t do. You are not able to do this clinically so when you have that scenario with fever you need to treat these patients as if they have meningococcemia. Now this is not only due to EcHO-9. You see this with multiple other enteroviruses. Just to show you some pictures. These almost ulcerative purpuric lesions look like meningococcemia. This is a child with a coxsackie A-9 infection. This by comparison is a child with meningococcemia. So the message is that you can have these enterovirus exanthems even without meningitis and they look like meningococcemia, and you need to treat them as if they were. You can’t differentiate them and sometimes, for example at Ft. Leonard Wood, actually both were circulating at the same time and there were cases that had meningococcemia during the outbreak of EcHO type 9 disease.
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Kawasaki Syndrome

Jammy B. — Thu, 10 Apr 2008 14:07:26 +0000

Kawasaki’s disease is a disease of unknown etiology. The manifestations relate to super-antigen formation and it is a multi-system inflammatory disease. And the main thing is fever of five days or more and then four of the remaining five manifestations. The definition is a surveillance definition and I think one of the take-home messages is that you should be prepared, in young children, to treat patients even though they don’t have four or five of the manifestations. There are certain things that just seeing it alone, and that is changes in the extremities, edema, induration of the hands and feet, is enough to strongly suspect Kawasaki’s disease if you don’t have another etiology.
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Other findings are conjunctival injection, mouth lesions, fissuring, crusting of the lips, strawberry tongue. The induration of the hands and feet in a child under a year is diagnostic in itself. Rash of quite variability and the least common manifestation is enlarged lymph nodes, even thought the original description included lymph nodes in the title. Associated with this is evidence of multi-system pyuria, various other findings. Important is aseptic meningitis and this should help you with the diagnosis, not turn you away from the diagnosis such as I have seen in one case.
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This is a picture and the rash can be multiforme, it can be just erythematous maculopapular, more important thing here is the swelling of the hands. The scleral conjunctivitis. This is late in the illness, the desquamation in the tips of the fingers and this is desquamation in the feet. This is the red palm, one of the original papers from Japan. Strawberry tongue in a Kawasaki’s patient. Now the crucial thing here, or the main problem with Kawasaki’s disease, are giant aneurysms of multiple different arteries, and the important ones are coronary arteries leading to infarcts. So patients need to be treated and you need to make a decision. With fever for a few days you have a lot of differentials of which Kawasaki’s is sort of at the bottom. Once you get beyond five days there are less differential possibilities and you want to treat by ten days. Human growth hormone information

Treatment is IVIG, and the most usual treatment today is 2 gm/kg over 12 hours. Also for inflammation, aspirin in high dose, four doses a day at 100 mg/kg. Then later put the patient on long-term aspirin for the anticoagulant effect. There are differences in this but certainly you need to wait until evidence of acute inflammation is over. There is no evidence that aspirin has any benefit as far as the heart is concerned, but there is evidence that IVIG treatment is beneficial. The other thing is that one dose is frequently not enough, so roughly 25% of patients need one or more doses, particularly in the children under a year.