Tweet
Chikungunya revisited
Chikungunya revisited
The Chikungunya (CKG) epidemic took Sri Lanka more by storm than by surprise toward the final quarter of 2006, for this viral infection has, in fact, been around in Southeast Asia and Africa for many, many years.
The countries affected included India, Thailand, Vietnam, Myanmar, Indonesia, the Indian Ocean Islands (in particular Re-union Islands) and East Africa.
The first recorded epidemic of this viral affliction, in 1952, was in Tanzania.
Similar epidemics were also reported in Bangkok (1960), India (1964), Sri Lanka (1965), Vietnam and Myanmar (1975), Indonesia (1979), returning to India in 2006 and, from October last year, also to Sri Lanka.
In Sri Lanka, the illness was initially described in 1965 as a clinical and a haematological entity by astute physicians investigating a viral illness strikingly similar to dengue then raging in Colombo.
The origins of the current outbreak of the epidemic in the country can be traced to Tanzania, from where it spread to Bangkok, then to India and - via Kerala - to Mannar, Jaffna, Batticaloa, Kalmunai, Puttalam and Colombo.
The highest number of infections reported so far in Sri Lanka was from Puttalam.
The explosive nature of the latest epidemic is perhaps attributable understandably to the lack of natural immunity in the country?s population as a whole, considering that the previous ?visitation? of this virus goes back over forty years.
There is also the possibility of the virus in the intervening period having mutated to acquire a heightened degree of virulence, resulting not only in the higher rates of infection reported but also in severity as well as the unusual manifestations reported this time round.
The animal hosts of the virus are monkeys and baboons. Once ingested by the mosquito, the virus replicates in the gut of the carrier.
The mosquito remains infective throughout its life-cycle which is about 6 weeks.
When an infected mosquito bites a human, the virus transfers into the bloodstream, multiplies in the endothelial cells and spreads to the other tissues in the human body such as the joints. Aedes Egypti and Albopictus, mosquitoes that feed during the day, help spread the Chikungunya infection.
Chikungunya affects all age groups. It begins with a sudden and acute onset of fever accompanied by chills and shivering which last for about three days, and causing severe muscle and joint pains. Loss of appetite is pronounced and may be accompanied by vomiting and loose motions. There may be large, red, extremely tender patches on the shins (like erythema nodosum/cellulitis) or a reddish rash similar to measles on the body, ulcers in the mouth, flushing of the face and redness of the eyes. There may also be swelling and tenderness over veins, particularly on the lower limbs.
All the above-mentioned ?symptoms? may or may not be manifest in all victims; in fact, a mild infection ? or what is known as an asymptomatic attack - could even pass unnoticed.
The treatment recommended is two Paracetamol tablets six-hourly and bed rest, with plenty of fluids taken orally. Should there be vomiting, or if dehydration is detected, the patient may need to have fluids administered intravenously.
Two to four weeks after an acute attack some patients develop a post-viral arthritis involving any joint in the body, with early morning stiffness.
There may be episodic recurrences of joint pains. Itching of the body and desquamation of the skin is also common at this stage.
Patients have been known to display signs of peripheral neuritis, facial palsy, foot-drop, carpal tunnel syndrome, ataxia, loss of balance and memory loss.
These are clinical observations and have not been established through biochemical and nerve conduction studies.
Fortunately Paracetamol and NSAIDs, though not curative, are known pain-relievers.
The use of Chloroquin and steroids has also been suggested, but there is no established clinical evidence to support resort to these modalities of treatment.
Joints, having a history of previous injury, and those often used in a repetitive fashion, seem more likely to develop arthralgia.
As regards investigations, a full blood count and liver enzymes test is advised.
The platelet count may be low like in dengue fever, as is the white cell count.
The specific tests needed are PCR for viral antibodies at the onset of the illness and Chikungunya (CKG) antibodies five days after the onset of the illness.
This description of the illness is from personal experience, the history derived from patients and from discussions with doctors involved in treating CKG patients. It is neither meant nor claimed to be evidence-based medicine.
The good news is that though CKG may be a long, smouldering illness, there is no evidence up to now of chronic sequelae.
The best news, however, is that immunity from CKG lasts a lifetime.
By Dr Selvie Perera ? fellow-victim
The Chikungunya (CKG) epidemic took Sri Lanka more by storm than by surprise toward the final quarter of 2006, for this viral infection has, in fact, been around in Southeast Asia and Africa for many, many years.
The countries affected included India, Thailand, Vietnam, Myanmar, Indonesia, the Indian Ocean Islands (in particular Re-union Islands) and East Africa.
The first recorded epidemic of this viral affliction, in 1952, was in Tanzania.
Similar epidemics were also reported in Bangkok (1960), India (1964), Sri Lanka (1965), Vietnam and Myanmar (1975), Indonesia (1979), returning to India in 2006 and, from October last year, also to Sri Lanka.
In Sri Lanka, the illness was initially described in 1965 as a clinical and a haematological entity by astute physicians investigating a viral illness strikingly similar to dengue then raging in Colombo.
The origins of the current outbreak of the epidemic in the country can be traced to Tanzania, from where it spread to Bangkok, then to India and - via Kerala - to Mannar, Jaffna, Batticaloa, Kalmunai, Puttalam and Colombo.
The highest number of infections reported so far in Sri Lanka was from Puttalam.
The explosive nature of the latest epidemic is perhaps attributable understandably to the lack of natural immunity in the country?s population as a whole, considering that the previous ?visitation? of this virus goes back over forty years.
There is also the possibility of the virus in the intervening period having mutated to acquire a heightened degree of virulence, resulting not only in the higher rates of infection reported but also in severity as well as the unusual manifestations reported this time round.
The animal hosts of the virus are monkeys and baboons. Once ingested by the mosquito, the virus replicates in the gut of the carrier.
The mosquito remains infective throughout its life-cycle which is about 6 weeks.
When an infected mosquito bites a human, the virus transfers into the bloodstream, multiplies in the endothelial cells and spreads to the other tissues in the human body such as the joints. Aedes Egypti and Albopictus, mosquitoes that feed during the day, help spread the Chikungunya infection.
Chikungunya affects all age groups. It begins with a sudden and acute onset of fever accompanied by chills and shivering which last for about three days, and causing severe muscle and joint pains. Loss of appetite is pronounced and may be accompanied by vomiting and loose motions. There may be large, red, extremely tender patches on the shins (like erythema nodosum/cellulitis) or a reddish rash similar to measles on the body, ulcers in the mouth, flushing of the face and redness of the eyes. There may also be swelling and tenderness over veins, particularly on the lower limbs.
All the above-mentioned ?symptoms? may or may not be manifest in all victims; in fact, a mild infection ? or what is known as an asymptomatic attack - could even pass unnoticed.
The treatment recommended is two Paracetamol tablets six-hourly and bed rest, with plenty of fluids taken orally. Should there be vomiting, or if dehydration is detected, the patient may need to have fluids administered intravenously.
Two to four weeks after an acute attack some patients develop a post-viral arthritis involving any joint in the body, with early morning stiffness.
There may be episodic recurrences of joint pains. Itching of the body and desquamation of the skin is also common at this stage.
Patients have been known to display signs of peripheral neuritis, facial palsy, foot-drop, carpal tunnel syndrome, ataxia, loss of balance and memory loss.
These are clinical observations and have not been established through biochemical and nerve conduction studies.
Fortunately Paracetamol and NSAIDs, though not curative, are known pain-relievers.
The use of Chloroquin and steroids has also been suggested, but there is no established clinical evidence to support resort to these modalities of treatment.
Joints, having a history of previous injury, and those often used in a repetitive fashion, seem more likely to develop arthralgia.
As regards investigations, a full blood count and liver enzymes test is advised.
The platelet count may be low like in dengue fever, as is the white cell count.
The specific tests needed are PCR for viral antibodies at the onset of the illness and Chikungunya (CKG) antibodies five days after the onset of the illness.
This description of the illness is from personal experience, the history derived from patients and from discussions with doctors involved in treating CKG patients. It is neither meant nor claimed to be evidence-based medicine.
The good news is that though CKG may be a long, smouldering illness, there is no evidence up to now of chronic sequelae.
The best news, however, is that immunity from CKG lasts a lifetime.
By Dr Selvie Perera ? fellow-victim