Symptoms of H5N1 (and other nasty strains)

kemosabe

Doooooooooom !
Hi all.. I just wanted to say I think there should be a thread pinned at the top of this side forum for symptoms of this bird flu... I havent seen anything yet on it..

thank you



PS ediited to ADD

only think i could find is the following



What are the symptoms of bird flu in humans?
Symptoms of bird flu in humans have ranged from typical flu-like symptoms (fever, cough, sore throat and muscle aches) to eye infections, pneumonia, severe respiratory diseases (such as acute respiratory distress), and other severe and life-threatening complications. The symptoms of bird flu may depend on which virus caused the infection


courtesy of the cdc website
 
Last edited by a moderator:

OddOne

< Yes, I do look like that.
I'll pin this up top and edit your subject to make it the symptoms thread - hopefully some others will wander by and clarify for us all.

The biggest thing I can see being a problem is the fact that all influenzas seem to hit people in about the same manner - even if the flu in question is a superflu. Distinguishing H5N1 from a garden-variety "normal" flu strain, and doing so early enough to do some good - may be impossible.

oO
 

Mrs. Peavey

Membership Revoked
Oddone,
I agree. From what I've read, the avian flu in humans begins in much the same manner as any other flu - aches, chills, fever, congestion, sore throat. But the difference is that within a matter of hours from the onset of these symptoms, the avian flu quickly evolves into compromising the lungs.
 

marsh

Has No Life - Lives on TB
I have read that this one has a longer incubation period, starts with diarhea and ends with deep lower lung involvement.
 

LMonty911

Deceased
hot off the press-

http://www.curevents.com/vb/showthread.php?t=24515&highlight=%24%24%24

5. The clinical spectrum of human H5N1 infections
At presentation, most cases of human H5N1 infections were characterized by a severe influenza syndrome, clinically indistinguishable from severe human influenza, with symptoms of fever, cough and shortness of breath, and radiological evidence of pneumonia (Chotpitayasunondh et al., 2005, Tran et al., 2004 and Yuen et al., 1998). Abnormalities on chest radiographs at presentation included extensive, usually bilateral infiltration, lobar collapse, focal consolidation, and air bronchograms. Radiological evidence of pulmonary damage could still be observed in surviving patients several months after the illness. Beside respiratory symptoms, a large proportion of patients also complained of gastrointestinal symptoms such as diarrhea, vomiting, and abdominal pain, which are common in children with human influenza, but not in adults. In some cases, diarrhea was the only presenting symptom, preceding other clinical manifestations (Apisarnthanarak et al., 2004 and de Jong et al., 2005). Unlike human infections with H7 or H9 viruses, conjunctivitis was not prominent in H5N1-infected patients. The clinical course of the illness in severe cases was characterized by rapid development of severe bilateral pneumonia necessitating ventilatory support within days after onset. Complications included acute respiratory distress syndrome, renal failure, and multi-organ failure. Evidence that the clinical spectrum of human H5N1 infections is not restricted to pulmonary symptoms was provided by a reported case of possible central nervous system involvement in a Vietnamese boy who presented with diarrhea, followed by coma and death. Influenza H5N1 virus was isolated from throat, rectal, blood, and cerebrospinal fluid specimens, suggesting widely disseminated viral replication (de Jong et al., 2005). His sister had died of a similar illness 2 weeks earlier, but no diagnostic specimens were obtained. Although highly virulent H5N1 viruses have shown neurotropism in mammals such as mice and cats (Keawcharoen et al., 2004, Lipatov et al., 2003 and Tanaka et al., 2003), these cases may be similarly rare as central nervous system manifestations associated with human influenza (Morishima et al., 2002 and Sugaya, 2002). Genetic predisposition of the host to such manifestations may play a role.

Striking routine laboratory results in H5N1-infected patients, especially in severe cases, were an early onset of lymphopenia, with a pronounced inversion of the CD4+/CD8+ ratio, thrombocytopenia and increased levels of serum transaminases (Chotpitayasunondh et al., 2005, Tran et al., 2004 and Yuen et al., 1998). High levels of cytokines and chemokines have been observed in several H5N1-infected patients, suggesting a role of immune-mediated pathology in the pathogenesis of H5N1 infections (Peiris et al., 2004 and To et al., 2001). This was supported by pathological examination in two patients who died during the outbreak in Hong Kong, which showed reactive hemophagocytosis as the most prominent feature (To et al., 2001). Other findings included diffuse alveolar damage with interstitial fibrosis, hepatic central lobular necrosis, acute renal tubular necrosis, and lymphoid depletion. Although the gastrointestinal, hepatic, renal, and hematologic manifestations could suggest wider tissue tropism, there was no evidence of viral replication in organs outside the respiratory tract (To et al., 2001). However, viral replication in the gastrointestinal is strongly suggested by reported virus isolation and detection of positive strand viral RNA from fecal specimens (de Jong et al., 2005 and Uiprasertkul et al., 2005).

While many laboratory-confirmed H5N1 infections were associated with severe, often fatal disease, milder cases have also been reported, especially during the outbreak in Hong Kong (Chan, 2002 and Yuen et al., 1998). An increasing number of milder cases also seemed to occur in Viet Nam, as the outbreak progressed in 2005 (WHO, 2005). While increased clinical awareness and surveillance may account for such observations, progressive adaptation of the virus to humans is the dreaded alternative explanation. The occurrence of mildly symptomatic and asymptomatic infections have also been suggested during the outbreak in Hong Kong by seroepidemiological studies in household members of H5N1-infected patients and health care workers. In these studies, 8 of 217 exposed and 2 of 309 non-exposed healthcare workers were seropositive for H5N1-specific antibodies (Bridges et al., 2002). Seroconversion was documented in two exposed nurses, one of whom reported a respiratory illness 2 days after exposure to an H5N1-infected patient. More importantly than showing the occurrence of asymptomatic infections, these data indicated that nosocomial person-to-person transmission had occurred, albeit limited to a few cases. An additional case of possible human-to-human transmission during the Hong Kong outbreak was suggested by H5N1-seropositivity in a household contact of a patient, who had no history of poultry exposure (Katz et al., 1999). Seroepidemiological studies in health care workers involved in the care of H5N1-infected patients in Thailand and Viet Nam in 2004 have not shown evidence of person-to-person transmission, despite the absence of adequate infection control measures in the Vietnamese cohort at the time of study (Apisarnthanarak et al., 2005, Liem and Lim, 2005 and Schultsz et al., 2005). During the outbreak in Thailand in 2004, extensive epidemiological investigations have suggested person-to-person transmission from a child, who died of presumed H5N1 infection, to her mother who had no history of exposure to poultry and had provided prolonged unprotected nursing care to her daughter (Ungchusak et al., 2005). An aunt of the child may have been infected by the same route since her last exposure to poultry before infection had been 17 days, considerably longer than the estimated incubation period of 2–10 days. There have been several similar family clusters of H5N1 cases in Viet Nam, which have all ignited concerns about the possibility of human-to-human transmission, but most of which could be explained by common exposure to poultry. While there has been no evidence of efficient transmission of influenza H5N1 virus between humans to date, caution and detailed investigations remain warranted in case of any cluster of infections, especially in view of the relatively rapid evolution H5N1 viruses have exhibited in recent years.
 

Brooks

Membership Revoked
http://www.influenzareport.com/ir/cp.htm [excerpt]

Presentation

Initial symptoms of H5N1 influenza may include fever (typically > 38°C), headache, malaise, myalgia, sore throat, cough, and rhinitis (although upper respiratory symptoms may be absent), gastrointestinal manifestations and conjunctivitis (Yuen 1998, Chan 2002). All these symptoms are non-specific and may also be associated with the currently circulating human influenza virus subtypes, H1N1 and H3N2. In two reports, diarrhoea (Hien 2004) was a prominent feature along with shortness of breath (Hien 2004, Chotpitayasunondh 2005). Watery diarrhoea may be present well before pulmonary symptoms develop (Apisarnthanarak 2004). Another report describes a four-year-old boy with severe diarrhoea, followed by seizures, coma, and death, suggesting the clinical diagnosis of encephalitis - avian influenza H5N1 was later detected in cerebrospinal fluid, faecal, throat, and serum specimens (de Jong 2005).

Laboratory findings of patients with severe avian influenza H5N1 include leucopenia, lymphopenia, impaired liver function with elevated liver enzymes, prolonged clotting times, and renal impairment. The lymphocyte count appears to be the most valuable parameter for identification of patients who are at risk of progression to severe illness (Chan 2002).

Clinical Course

As of December 2005, about half of the patients diagnosed with clinical avian H5N1 influenza infection have died. Most of these patients had severe disease on admission to hospital. In patients with respiratory failure and fatal outcome, dyspnoea developed after a median of 5 days (range 1-16) in one series (Chotpitayasunondh 2005). Abnormal chest radiographs include interstitial infiltration, patchy lobar infiltrates in a variety of patterns (single lobe, multiple lobes, unilateral or bilateral distributions). Finally, the radiographic pattern progresses to a diffuse bilateral ground-glass appearance, with clinical features compatible with ARDS (Chotpitayasunondh 2005). In the report from Vietnam, major x-ray abnormalities include extensive bilateral infiltration, lobar collapse, focal consolidation, and air bronchograms. All patients had dramatic worsening of findings on chest radiography during hospitalisation. The median time from onset of fever to ARDS was 6 days (range 4-13) in one series (Chotpitayasunondh 2005). Pneumothorax may develop in patients during mechanical ventilation (Hien 2004). Pleural effusions are uncommon.

There is conflicting information as to the risk factors associated with severe disease and fatal outcome. In the 1997 outbreak in Hong Kong, the factors associated with severe disease included older age, delay in hospitalisation, lower respiratory tract involvement, and a low total peripheral white blood cell count or lymphopenia on admission (Yuen 1998). In this report, patients aged below 6 years usually had a self-limiting acute respiratory disease with fever, rhinorrhoea, and sore throat. In contrast, recent avian H5N1 infections have caused high rates of death among infants and young children (Chotpitayasunondh 2005). The numbers reported are too small to understand whether local factors - i.e., time between onset of symptoms and admission to hospital - or viral virulence factors are responsible for these differences. As H5N1 strains have evolved over the past 10 years (Webster 2006), clinical features of avian influenza infection in humans may well have different characteristics over time.

The progression of severe H5N1 infection seems to be different from that of severe diseases observed during earlier influenza pandemics. None of the patients with severe disease reported from Hong Kong (Yuen 1998) and Vietnam (Hien 2004) had evidence of secondary bacterial pneumonia, suggesting that the fatal outcome was due to an overwhelming primary viral pneumonia. This feature is reminiscent of the 1918 pandemic and may pathogenetically be due to a "cytokine storm" (Barry 2004).
 

Fuzzychick

Membership Revoked
All I say is this...I have connections to the hilt...it's acoming folks, being a nurse I know this but those that are in the KNOW have said up, it's imminent...no full panic being manned here, just a warning with alot of links to prepare.
One in particular is given to me is www.myherbs.com. There are other links esp to Chinese herbs, I post them shortly, I've been going thru them. STOCK UP AND PREPARE as I know you all do. FC
 

susie_q

Veteran Member
FC,

I don't refute what you say; rather, am curious why you say it's coming. Frankly, I expected to see fallout by now, in light of migration to Alaska and south from there. WA State is testing birds and has been since August (I believe). Can you share why you say "it's coming"? Please understand I'm not demanding that you do, just hoping for some clarification. :)
 

Keesha

Contributing Member
I was just in to see my family doctor this week. Last week he had been to a Doctors health conference of some kind in Washington DC. He too said it is coming. Be prepared is what he said. He sounded like we should be prepared also for no electricity since he suggested having at least 2 weeks worth of food and water stored plus the fiber paint masks for the caregivers and for use if you have to get out of the house and are not quarantined.He suggested to be prepared with fever reducers, cough syrups, etc...He fully expects the population in the US to be drastically reduced with this.
 

LibertyWeeps

Inactive
All I say is this...I have connections to the hilt...it's acoming folks, being a nurse I know this but those that are in the KNOW have said up, it's imminent...no full panic being manned here, just a warning with alot of links to prepare.
One in particular is given to me is www.myherbs.com.

http://news.yahoo.com/s/ap/20090830/ap_on_he_me/us_med_swine_flu;_ylt=AvPShP7_OE9wWm5VT522l.6s0NUE;_ylu=X3oDMTMyMGMybTVtBGFzc2V0A2FwLzIwMDkwODMwL3VzX21lZF9zd2luZV9mbHUEY3BvcwM3BHBvcwM0BHB0A2hvbWVfY29rZQRzZWMDeW5faGVhZGxpbmVfbGlzdARzbGsDcmV0dXJub2Zzd2lu

NOTICE THE AGE GROUPS.?! VACCINES GONE WRONG? GENETIC ENGINEERING? CHEMTRAILS OR JUST A SCARE ON A GLOBAL SCALE. W.H.O. HAS A LOT OF CLOUT
 

GarnetRooster

Contributing Member
Got the flu Thursday afternoon. Was fine until about 4:30 PM. Went to the doc Friday morning. 102.2 temp, coughing my head off and a headach. Fever finally broke at 12:00AM.
 

Signwatcher

Veteran Member
Is it myherbs.net, Fuzzychick? Because I don't get anything coming up on the .com site you posted. And just WHICH herbs are good for flu?
 

summerthyme

Administrator
_______________
Signwatcher- this is an OLD thread (like, SIX YEARS old!!)

Fuzzychick (and about half the posters on the thread) are no longer here.

If you want to know which herbs are good for flu, look at other threads here or do a search. We've certainly detailed natural treatments for influenza many times here.

Summerthyme
 
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