//KHARA HAIS MUNICIPALITY
What is Congo-Crimean Haemorrhagic Fever?
The following is an extract from an article in the SAMJ, Vol. 62,
Congo-Crimean haemorrhagic fever
Congo-Crimean haemorrhagic fever was first observed in the Crimea by Russian
scientists in 1944 and 1945. At that time it was established by studies in human
volunteers that the aetiological agent was filtrable and that the disease in man
was associated with the bite of the tick Hyalomma marginatum. The agent
was detected in the larvae and in adult ticks, as well as in the blood of
patients during the fever. This agent, presumably a virus, was not maintained in
the laboratory and was lost.
The most important transmitters of the infection to man are species of the genus Hyalomma, the life history of which is shown in the figure below.
The infection is usually transmitted to man by the bite of a tick, but an increasing number of cases have occurred among the medical and nursing staff caring for patients in hospital and in laboratory personnel carrying out investigations of these patients. In these cases the infection has apparently been acquired by contagion, particularly by contact with the patient's blood or blood-contaminated specimens. Exposure to the blood of infected animals, especially cattle and sheep, has led to severe and often fatal infections.
The incubation period is 2 - 7 days. The onset of the illness is sudden, with fever, chills, severe muscular pains, headache, vomiting and pain in the epigastric and lumbar regions. A haemorrhagic state develops from the 3rd to the 5th day and manifests as petechial haemorrhages or purpura in the skin, and bleeding from the mucous membranes manifests as epistaxis, haemoptysis, haematemesis, melaena and haematuria. At this stage the conjunctivae are injected, the face is flushed and the tongue is dry, often coated with dry blood. The pulse is slow in the beginning, but with continuing loss of blood becomes fast and feeble; the blood pressure drops and the heart sounds become weak - clear signs of impending shock and vascular collapse. The liver is enlarged and tender and there is tenderness over the epigastrium and splenic region. In patients who recover, the temperature falls between the 10th and the 20th day and bleeding stops, but convalescence is prolonged up to 4 weeks or longer. In fatal cases, death from massive haemorrhage and cardiac arrest occurs, usually 7 - 9 days after the onset of the illness. Massive haemorrhage into the gastro-intestinal tract, with scattered haemorrhages into the viscera, is found at autopsy.
The diagnosis is suggested on clinical grounds when the patient has a history
of a tick bite or of exposure to ticks in the environment, and after an
incubation period of 2 - 7 days develops an illness of sudden onset of muscle
pains, headache fever and a rapidly evolving severe illness with the development
of a haemorrhagic state with bleeding from the mucous membranes and petechiae in
the skin, associated with thrombocytopenia and leucopenia.
The authors are grateful to Professor 0. W. Prozesky, Director of the National Institute for Virology, and to Dr R. Swanepoel, Dr K. Struthers, Mrs E. Rossouw and Miss G. McGillivray, staff members of the high-security laboratory, and to Dr P. Jupp of the Arbovirus Unit of the National Institute for Virology for undertaking, as a matter of urgency, the investigations which led to the incrimination of the Congo virus as the cause of this patient's fatal illness. The authors are grateful to Mrs M. Anderson, who prepared the chart of its life cycle.
This document was prepared by Professor Robert Swanepoel, and sent to the listserv "Promed" at the end of the out break.
Hi Dr Woodall
Sorry I have not been feeding you the latest news on the outbreak but:
Anyhow, now that you have asked I can answer the question about "bont" and give you some sort of update on the outbreak. Bont means multicoloured or variegated, and refers to the reddish-brown and white bands on the legs of ticks of the genus Hyalomma. Ticks of the genus Amblyomma resemble Hyalommas in some ways: they are of similar large size (relative to other ixodids), and have similar bands on the legs, but Amblyommas are altogether more ornate, with beautiful enamelling or metallic colours on the scutum, to gladden the heart of the most jaded acarologist. There is also a single (sub)species of the genus Rhipicephalus which can be confused with Hyalommas by the uninitiated: Rhipicephalus evertsi mimeticus - the mimeticus part refers to the fact that it mimics Hyalommas in having the banded leg ornamentation, but it lacks the relatively long mouth parts of Hyalommas, Amblyommas, or even Aponommas (you asked!).
The late Harry Hoogstraal in his extensive reviews of the literature made reference to the fact that the world distribution of CCHF virus coincides pretty well with the distribution of Hyalomma ticks (Africa, eastern Europe and Asia), and indeed this became even more true after his last review as we found that the virus occurs down the length of Africa, and it was likewise found to occur across Asia to China (note, I did not say that the distribution has extended, or that the virus has spread etc - only our knowledge of it). Other ticks can transmit, but there seems to be a particular link with Hyalommas, and this has certain epidemiologic consequences, relating for instance to the host preferences of the immature and adult ticks, which differ from ticks of other genera: larvae and nymphs feed on small mammals up to hare size and ground-frequenting birds, while adults prefer large animals, the larger the better. This means humans are not bitten by the immatures ("seed" or "pepper" ticks) of Hyalommas (humans are bitten by the immatures of other ticks) and even the adults are not that partial to humans, although they do bite if given good reason. If this all were otherwise, and Hyalommas loved feeding on humans, we would be in a sorry mess for antibody surveys on livestock sera show that we live in a sea of CCHF virus within the distribution range of Hyalommas, and the miracle is that there are so few human cases, not that there are so many.
Humans gain infection from tick bite (yes, the occasional Hyalomma), or from contact of infected fresh blood (or other tissues) with broken skin - with the infected blood/tissues coming either from human patients (nosocomial infections - needle sticks etc), or other animals, commonly sheep and cattle. To our knowledge, only humans and newborn mice readily succumb to disease; other animals including nonhuman primates are either refractory or undergo mild infection, sometimes with transient viraemia - including sheep and cattle (our unpublished results). Sheep and cattle are viraemic for up to about a week, and often exposure to ticks and virus infection occur at an early age, when farmers may castrate, dehorn, stick in ear tags or immunize the young animals, and thus expose themselves through getting infected blood onto broken skin. Sometimes animals meet tick infestation for the first time late in life and then succumb to tick-borne diseases of livestock such as babesiosis or anaplasmosis, at the same time that they happen to have first met CCHF virus, and are thus viraemic at a time when they are treated, autopsied, or even butchered by farmers, veterinarians or farm workers respectively, and this constitutes another type of incident leading to common source outbreaks. Most often then, the disease affects stockmen and other farm dwellers, and townspeople only become infected when they visit the countryside and get tick bite, or hunt and slaughter animals etc. It is also enough to squash infected ticks with bare fingers - one does not have to be bitten. The only town dwellers who are regularly exposed to infection are slaughtermen at abbatoirs - since they encounter fresh blood and other tissues of livestock (commonly sheep and cattle) hundreds of times daily - sometimes more than a thousand head of sheep or cattle a day, they must come across animals in the short viraemic phase of infection fairly often, and we know they get the disease more frequently than other people, and it seems, also relatively mild/silent infections with seroconversion - all the same, there would probably be many more abbatoir infections if the viraemia in livestock were more intense than it is - very low-titered in comparison with Rift Valley fever for instance. Ticks which detach from hides and skins at slaughterhouses after their engorgement has been so rudely interrupted, will sometimes attach to whatever is available, and this constitutes another hazard for abbatoir workers.
What then of risk for the urban consumer of meat? In 17 years of looking at about 2000 cases of suspected viral haemorrhagic fever, we have never found CCHF in a town dweller who did not have a history of recent tick bite, or animal blood contact in the countryside or at an abbatoir, nor were we able to isolate virus from meat from experimentally infected sheep killed in viraemia. The virus is not very resistant to heat and pH extremes etc, and we assume the fall in pH associated with "maturation" of meat by hanging of carcases after slaughter, is sufficient to put paid to residual virus after "bleeding out" of the animal at slaughter.
Having said all that, we come to Oudtshoorn, the centre of an ostrich industry which sells (locally and abroad), feathers, skins and meat. An ostrich farmers' co-operative runs several slaughterhouses, and these resumed slaughtering (after an off season) on 21 October. (Two of the abbatoirs are in Oudtshoorn.) By pure coincidence a survey was undertaken at the largest of the abbatoirs of the tick burden (mainly Hyalomma truncatum) on birds coming in from various farms, and it was found that six consignments were heavily infested. This is the slaughterhouse where the outbreak occurred. As far as I know at present - and the dust has not yet settled properly - abbatoir workers started becoming ill from about Sunday 27 October to Wednesday 30, and being admitted to Oudtshoorn Hospital from Thursday 31 to Saturday 2 November, and on Sunday 3 November four patients were transferred to Tygerberg Hospital, Bellville, near Cape Town. We received serum samples from these four on Monday 4 November afternoon, and that evening confirmed that three had IgG and IgM antibodies to CCHF virus, and that the fourth was PCR positive for viral nucleic acid. Meantime media hysteria mounted and, I think, hundreds of worried folk presented with varying degrees of "symptoms" - I think there are something like 350 workers at the abbatoir, but all will be known later. Various people were admitted to Oudtshoorn, including a forty six year old lady who died on Monday 4 November (she was an abbatoir worker and has been cremated) - we received only formalin fixed bits of liver taken with a biopsy needle - this was last night (Wed 6 Nov) and we are awaiting preparation of histo sections to perform immunocytochemical staining.
Meantime a further 12 or so patients were transferred to Tygerberg, I think Tues evening, and we received serum samples from 13 patients (over and above repeat bleeds on the original four) last night and this afternoon. Of these thirteen, 11 were IgG and IgM positive, and two negative for antibody and PCR (one of these was not really a patient - simply an abbatoir worker who pitched up at hospital to visit somebody else and was bled for her troubles). So, Dr Mark Beale at Tygerberg Hospital who is in over all control of the clinical side of things, and his supporting workers at both centres, seem to have done a very good job of sorting the sheep from the goats, and the fourteen antibody positive patients are to be discharged tomorrow (Friday 8 Nov). The original PCR positive patient who lacked antibodies remains PCR positive, antibody negative, and still has low platelets, but seems well. He will be detained in Tygerberg for the meantime, as will one of the two PCR and antibody negative people who seems quite ill (the other was the hospital visitor who was not ill or admitted). All of the above patients were abbatoir workers. I am not sure who remains in Oudtshoorn Hospital, but there are two children from whom we await specimens - one is, and both may be, children of abbatoir workers, and it is thought that one in fact has hepatitis A (or B?).
All of the abbatoirs were closed and we are approaching the end of the theoretical incubation period when we can expect further primary common source cases - there appear to have been no secondary (human-to-human cases) unless either or both of the two children prove to be cases. It will take a further while to make virus isolations, but antibody detection and PCR have done a splendid job of rapid laboratory confirmation for us. To summarize: 14 seropositive patients are all well, and ready to be discharged; one deceased probable case is still to be confirmed by immunocytochemistry, one PCR positive antibody negative patient is off the critical list but still in hospital, and one PCR negative and antibody negative patient (who may or may not prove to be a case) is still in hospital, as are two children. Excluding the children, 10 of the patients are female (including the deceased), and most are young adults - the high proportion of females relates to the fact that many females are employed in the ostrich abbatoirs as compared to sheep and cattle abbatoirs.
Prof James Joubert at Tygerberg Hospital has arranged for Dr Neil du Toit, seconded form Tygerberg, to bleed (subject to necessary consent etc) all abbatoir workers and we shall test for evidence of mild, or past, or inapparent infections. I have advised that farmers should have a section of their feedlots double fenced, the inner fence to be small animal proof, and that ostriches should be treated with a short half life pyrethroid acaricide (non residual) 14 days before being sent for slaughter and placed in the fenced off "quarantine" section for this period - they should then arrive at the slaughterhouse tick and virus and acaricide free, by analogy with sheep and cattle experiments, but we still have to do ostrich experiments. Pyrethroids in any event have very rapid "knockdown" (lethal) effect on ticks, and very low mammalian toxicity. The Directorate of Veterinary Public Health and ostrich farmers' co-ops and research organizations have met to discuss the problem, and will act something on the lines I have suggested. Meanwhile Dr Willem Burger of the ostrich producers research lab has sent us ten half grown chicks (tick free) to do experimental viraemia studies etc (they are big enough to look you in the eye, and they defaecate a bucketful - any volunteers to help us?) I shall be visiting the area hopefully next week and with Dr Burger visit farms to collect ticks etc. From our sheep and cattle surveys we know that the virus is everywhere, and while we are not trying to incriminate anybody, it will be interesting to see if we can get virus isolates from ticks to match up by nucleotide sequencing with any isolates from patients. (The fact that most infections have been relatively benign is interesting of itself).
Incidentally, there was a worker at an ostrich slaughterhouse near Oudtshoorn who became infected in 1984 - he claimed that Hyalomma ticks on ostriches scratched his hands and arms as he pulled off the skins from the birds, and we thought that was one possible way of becoming infected. Another would be ticks transferring to the slaughtermen after detachment from ostrich skins, and of course, another possibility is that ostriches can become viraemic - which we are setting out to investigate now. We previously failed to obtain ostriches to experiment on, and tested guinea fowl and chickens - which were fairly resistant to the virus - but they may be quite different from ostriches which, I think, may have a slightly different thermoregulatory capacity from other birds, for one thing.
I hope I have for once and all cured you of asking me questions.
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