this presentation put insights on the most important pivots of the Crimean-Cong Hemorrhagic Fever in Iraq and the World and was a part of institutional efforts represented by University of Misan/Iraq as step of many steps to educate community to this dangerous zoonotic disease.

1. Crimean-Congo Hemorrhagic Fever: The
Epidemiology and Control Approaches
Presented by:
Dr. Zahid S. Aziz
1

2. • Presentation outlines:
• Definition
• History and epidemiology
• virus characteristics
• Effects of environmental conditions on viral transmission
• Reservoirs and vectors
• Signs and symptoms
• Population genetics
• Outbreaks
• Pathology(biochemical and immunological parameters)
• Diagnosis
• Treatment and control
• Crimean-Congo Hemorrhagic Fever - Iraq
2

3. The term of viral hemorrhagic fever (VHF)
designates a group of diseases, caused by
enveloped RNA viruses from four different virus
families (Arenaviridae, Filoviridae, Bunyaviridae
and Flaviviridae is acquired through contact with
animals or the bite of an infected arthropod. At least
14 different viruses belonging to these families were
defined as the cause of VHF
3

4. Crimean-Congo hemorrhagic fever (CCHF),
a tick-borne viral hemorrhagic fever, is a
zoonotic infection that caused by CCHF
virus (CCHFV) of the family Bunyaviridae,
genus Nairovirus. Transmission occurs
mainly by Hyalomma m. marginatum tick
exposure. Blood and bloody excretions of
the patients are highly infectious and
contact of skin and mucous membrane
may lead to CCHF transmission. CCHF was
described firstly in the Crimean peninsula
in 1944, in former Soviet Union
4

5. History, epidemiology
The disease was described firstly in the Crimean
peninsula in 1944 during an outbreak, which in-
volved more than 200 cases and was called as
Crimean hemorrhagic fever. Afterwards, the virus
isolated in the Democratic Republic of Congo in Af-
rica was noted to be the same pathogen, resulting
in the name of CCHFV.7 Until now, CCHF infection
has been reported in countries of Asia, the Middle
East, Southeastern part of Europe and Africa.
5

6. virus characteristics
A common feature of this family is the genome, consisting
of three segments of single stranded RNA, referred to as
the S, M and L segments. The S segment encodes the viral
nucleo capsid protein (NP), M the glycoproteins (GN and
GC), and L the RNA dependent RNA polymerase.
A CCHFV virion is spherical, ~100 nm in diameter, and has
a lipid bilayer envelope ~5-7 nm thick, through which
protrude glycoprotein spikes 8-10 nm in length. The
glycoproteins are involved in adhesion to their receptors
in mammalian cells. Virus is then taken into the cell by
endocytosis. Viral replication occurs in the cytoplasm,
endoplasmic reticulum and the Golgi apparatus and then
the virus is released from cells
6

7. To date the receptor of CCHFV in target cells is not
known. The viral glycoproteins Gn and/or Gc are involved
in the initial attachment of CCHFV to the cell plasma
membrane. It was suggested that Gc is responsible for
binding to the cellular receptors, and mediates fusion
later, during the early step of replication cycle. An
interaction between CCHFV glycoproteins and cell surface
nucleolin, a protein found predominantly within nucleoli,
has been suggested as putative entry factor
7

8. 8

9. 9

10. Effects of Environmental conditions on viral transmission
It is believed that the CCHF epidemics occur in Eastern
Europe and Asia because of the changes of environmental
conditions by humans. The first CCHF epidemic in the
Crimean peninsula, during the World War II occurred due
to opening of the tick infected regions to agriculture. CCHF
epidemics in former Soviet Union and Bulgaria are related
to the politics of agriculture and farming of both countries.
Regions with warm climate and highly fragmentation of
the landscape vegetation are suitable habitats for
Hyalomma ticks and correlate with high risk
10

11. Changes in ecological conditions such as an increase in bush land, as a
consequence of a neglected use of agricultural land or of deforestation
measures to gain farmland, contributed to an increase in proper habitats for
Hyalomma ticks and their reservoir animals. The disease has a seasonal
character. In the Northern hemisphere, the highest number of CCHF cases is
reached from June to July. In Turkey, the cases become evident in March and
continue to the end of September month. In the Southern hemisphere the
majority of cases occur in Spring and Autumn. CCHF appearance varies
according to geographical regions and can also be seen in January related to
tick movements. In addition to ticks, animals play crucial roles in the life
cycle of ticks particularly in transmission and amplification of the virus.
Although viraemia in animals can continue for two weeks, they do not show
any clinical signs of CCHF. The CCHF transmission occurs mainly by tick
exposure namely by tick bite and crushing infected ticks and direct contact
with blood or other infected animal or human tissues. Intrauterine or
perinatal CCHF transmission from mother to baby may also occur.
Agricultural workers, animal raisers, veterinarians, those who are in contact
with sick animals, healthcare workers in CCHF endemic areas, soldiers, and
campers are at high risk for CCHF infection
11

12. CCHFV previously has been isolated from more than 30
ticks including Hyalomma anatolicum anatolicum,
Hyalomma truncatum, Hyalomma marginatum rufipes,
Hyalomma impeltatum, Hyalomma impressum,
Amblyomma variegatum, Boophilus decolaratus and
Rhipicephalus, Ornithodoros, Dermacentor and Ixodes
species. Some of those ticks have not been proven to be
the biological vector yet even if the virus is isolated from
the ticks. It is well known that the spread of CCHFV in a
region primarily coincides with the spread of Hyalomma
ticks. Ticks are not only vectors for CCHFV but also
natural reservoirs since the virus can be transmitted
transstadially, transovarially or by venereal route within
the tick population
12

13. Ticks are both "environmental reservoir" and vector for the
virus, carrying it from wild animals to domestic animals and
humans. Tick species identified as infected with the virus
include Argas reflexus, Hyalomma anatolicum, Hyalomma
detritum, Hyalomma marginatum
marginatum and Rhipicephalus sanguineus. At least 31
different species of ticks from the
genera Haemaphysalis and Hyalomma in southeastern Iran
have been found to carry the virus Wild animals and small
mammals, particularly European hare, Middle-
African hedgehogs and multimammate rats are the
"amplifying hosts" of the virus. Birds are generally resistant to
CCHF, with the exception of ostriches. Domestic animals like
sheep, goats and cattle can develop high titers of virus in their
blood, but tend not to fall
ill
13

14. The "sporadic infection" of humans is usually caused by
a Hyalomma tick bite. Animals can transmit the virus to
humans, but this would usually be as part of a disease cluster.
When clusters of illness occur, it is typically after people treat,
butcher or eat infected livestock,
particularly ruminants and ostriches. Outbreaks have occurred
in abattoirs and other places where workers have been
exposed to infected human or animal blood
and fomites Humans can infect humans and outbreaks also
occur in clinical facilities through infected blood and unclean
medical
instruments
14

15. 15
Birds are the main hosts for the immature stages of this tick
species (2). Viremia does not develop in most passerine birds
(3,4), which are not able to pass the virus to ticks. However,
migratory species could carry infected ticks over long distances
and thereby disseminate the virus (2)
401 animal sera (353 cow, 30 sheep, 10 goat and 8 chicken)
in four endemic municipalities in Kosovo. We detected
specific antibodies in all animals except in chicken.
Seroprevalence in cows is comparable to other endemic
areas and correlates to the seroprevalence in humans. No
CCHF RNA could be detected in 105 tick samples obtained in
2012 and 2013. .

16. 16
It has also been found in a number of species in the genera
Rhipicephalus, Boophilus, Dermacentor and Ixodes. How many of
these ticks are competent vectors is uncertain, but some might
transmit the virus locally. CCHFV has been reported infrequently in
other blood-feeding invertebrates, such as biting midges (Culicoides
spp.) and argasid (soft) ticks, but they are not thought to play any
role in its epidemiology. Experimental infections indicate that it
does not replicate in argasid ticks. Migratory birds might spread
infected ticks between distant regions. CCHFV in blood, tissues or
crushed ticks can enter the body after contaminating mucous
membranes or skin. Infections acquired through skin contact
probably occur via broken skin. Some cases appeared to be caused
by drinking unpasteurized milk, and a few were reported in people
who had recently eaten raw liver or raw meat from freshly
slaughtered animals. Person-to-person transmission can occur,
especially during close contact. Hemorrhages from severely ill
patients are an important source of exposure for relatives and
healthcare workers.

17. 17
Viral RNA has also been detected in saliva and urine, and intermittently and
in low amounts in conjunctival, nasal and rectal swabs. However, some
studies suggest that skin contact with secretions and excretions that do not
contain blood might have a relatively low risk of transmission. Sexual
transmission was proposed to be the source of the illness in a few cases,
including one instance where a man probably transmitted the virus to his
wife during convalescence. Airborne transmission has been reported rarely
after laboratory accidents or medical procedures that generated droplets or
aerosols. In one unusual outbreak, clinical cases occurred in several people
who visited the room of a severely ill patient who was on a respirator, but
had no direct contact with the patient. In utero transmission has been
reported in humans, but its frequency is unclear. Whether CCHFV can be
transmitted in milk is still uncertain, although no viral RNA was detected in
the milk of two mothers who breastfed until diagnosis, and their infants did
not become infected. Possible contamination of milk with blood (e.g., in skin
lesions) is a concern even if the virus is not secreted directly into milk. How
long CCHFV persists during convalescence is unclear. Nucleic acids have been
found in urine for up to 25 days after the onset of clinical signs, and in blood
for up to 36 days, but the presence of live virus was not demonstrated in
either case.

18. 18
Many birds are resistant to infection, but ostriches are
susceptible and may show a high prevalence of infection in
endemic areas, where they have been at the origin of
human cases. For example, a former outbreak occurred at
an ostrich abattoir in South Africa. There is no apparent
disease in these animals.
Animals become infected by the bite of infected ticks and
the virus remains in their bloodstream for about one week
after infection, allowing the tick-animal-tick cycle to
continue when another tick bites. Although a number of tick
genera are capable of becoming infected with CCHF virus,
ticks of the genus Hyalomma are the principal
vector.

19. 19
A total of 546 captured birds were checked for ticks, and parasites
were found on 21 birds from 5 passerine bird species
(Phoenicurus phoenicurus, Erythropygia galactotes, Iduna
opaca, Acrocephalus scirpaceus, and I. pallida). All but I.
pallida birds are passerine trans-Saharan migrant species, coming
from central and southern Africa and able to reach the Iberian
Peninsula.
A) Iduna opaca, B) Erythropygia galactotes, and C) Phoenicurus phoenicurus birds. D–G) Hyalomma
marginatum tick specimens removed from birds and preserved in alcohol: D) semi-engorged larva,
E) semi-engorged nymph, F) semi-engorged and fully engorged nymphs, and G) fully engorged
nymphs

20. 20
wild ground-feeding birds are frequently infested with immature ticks. In
two areas where numerous Crimean-Congo haemorrhagic fever (CCHF)
virus isolations were obtained from Hyalomma marginatum rufipes adult
ticks collected on ungulates, 175 birds were captured and sera collected.
CCHF antibodies were detected by ELISA in 6/22 red-beaked hornbills
(Tockus erythrorhynchus), 2/11 glossy starlings (Lamprotornis sp.) and
1/3 guinea fowls. The virus was isolated from H. m. rufipes nymphs
collected on a hornbill. The role of wild ground-feeding birds in
CCHFvirus ecology in West Africa is discussed
.
Tockus erythrorhynchus
‫طائر‬
‫البوقير‬
‫االفريقي‬
(Lamprotornis sp
‫الزرزور‬
guinea fowls
‫غينيا‬ ‫دجاج‬

21. 21
An experimental model for investigating the role of birds in the CCHF
virus transmission cycle was developed. Following CCHF virus
inoculation, antibodies were detected by enzyme-linked immunosorbent
assay in one red-beaked hornbill and one glossy starling, but not in two
laughing doves and six domestic chickens. None of the birds showed a
detectable viremia. Hyalomma marginatum rufipes larvae were placed
on three red-beaked hornbills and one glossy starling. These birds were
then inoculated with CCHF virus .Virus transmission to larvae or nymphs
was obtained and seroconversions in birds were recorded. Virus was
also detected in 90% of the individually tested nymphs, as well as in
adults. The virus was then successfully transmitted by adult ticks to
rabbits and the engorged females were allowed to oviposit. Progeny
larvae were placed on another group of birds and one of three birds
showed seroconversion. The cycle of transmission of virus between ticks
and a viremic ground-feeding birds represent a potential reservoir and
amplification mechanism of CCHF virus in
west
Africa.

22. 22

23. 23

24. Signs and symptoms
The clinical signs and symptoms of CCHF are similar to those of
other viral haemorrhagic fever infections, such as Ebola, Marburg
and Lassa. Its course is determined by the infective dose (MID: 1 –
10 viruses)
The clinical illness associated with CCHFV is a severe form
of hemorrhagic fever. Following infection by a tick bite, the incubation
period is typically two to three days but can last as long as nine days,
while the incubation period following contact with infected blood or
tissues is usually five to six days with a documented maximum of 13
days. The onset of symptoms ushering in the prehemmorhagic phase
is sudden, with fever, myalgia, (muscle ache), dizziness, neck pain
and stiffness, backache, headache, sore eyes and photophobia
(sensitivity to light). Typical symptoms include nausea, vomiting
(which may progress to severe bleeding and can be fatal if not
treated), diarrhea, abdominal pain and sore throat early in the acute
infection phase, followed by sharp mood
swings, agitations and
confusion
24

25. After several days, agitation may be replaced by sleepiness, depression
and lassitude, and the abdominal pain may localize to the upper right
quadrant, with detectable liver enlargement. As the illness progresses into
the hemorrhagic phase, large areas of severe bruising, severe
nosebleeds, and uncontrolled bleeding at injection sites can be seen,
beginning on about the fourth day of illness and lasting for about two
weeks. Other clinical signs include tachycardia (fast heart rate),
lymphadenopathy (enlarged lymph nodes), and a petechiae (a rash
caused by bleeding into the skin) on internal mucosal surfaces, such as in
the mouth and throat, and on the skin. The petechiae may give way to
larger rashes called ecchymoses, and other haemorrhagic phenomena.
There is usually evidence of hepatitis, and severely ill patients may
experience rapid kidney deterioration, liver failure or pulmonary failure
after the fifth day of illness.
25

26. Pathology(biochemical and immunological parameters)
Abnormalities are related to the severity of the infection. These include
leucopenia or leukocytosis, elevated liver enzymes (AST and ALT),
prolonged thrombin and activated partial prothrombin times and
elevated levels of fibrin degradation products. Bilirubin, creatinine and
urea are also raised in the second week of the acute phase
accompanied by a decline in serum protein levels, all indicating a
progressive loss of liver function. Histochemical and in situ
hybridisation shows involvement of both hepatocytes and endothelial
cells (Burt et al., 1997). Histopathological examination of the liver
reveals a lack of an inflammatory infiltrate, suggesting that the necrosis
in hepatocytes is the direct consequence of virus replication. Necrosis
ranges from spotty necrosis in the mid-zonal regions to massive
necrosis involving over 75% of the hepatocytes. Lesions in other organs
include haemorrhage, congestion and necrosis in the kidneys, CNS and
adrenals, accompanied by a general depletion of the lymphoid system.
Fibrin deposits may be seen within the blood vessels of these organs
26

27. 27
Vascular leakage may be caused either by destruction of endothelial
cells or by a disruption of the endothelial cell junctions. It is still
unknown whether vascular dysfunction is due to a direct effect of
virus on the endothelial cells or a consequence of a cytokine storm
Key players in disease progression are interleukin (IL)-10, IL-1, IL-6
and tumour necrosis factor-a (TNF-a). In vitro studies showed that
CCHFV replicates in human dendritic cells and macrophages resulting
in the release of TNF-a, IL-6 and IL-8, which then can activate
endothelial cells in vitro.
In contrast to milder CCHF cases, elevated levels of pro-
inflammatory mediators (such as TNF-, IL-6, IL-10) and serum
markers of vascular activation (sICAM-1 and sVCAM-1) have been
detected in fatal CCHF cases.
These clinical observations are mirrored in an in vitro experiment, in
which it was demonstrated that CCHFV infected endothelial cells can
up-regulate ICAM-1 and VCAM.
It was shown that CCHFV induces apoptosis in vitro late post
infection in human target cell lines

28. Population genetics
CCHFV is the most genetically diverse of the arboviruses: Its nucleotide
sequences frequently differ between different strains, ranging from a
20% variability for the viral S segment to 31% for the M
segment. Viruses with diverse sequences can be found within the same
geographic area; closely related viruses have been isolated from widely
separated regions, suggesting that viral dispersion has occurred
possibly by ticks carried on migratory birds or through international
livestock trade. Reassortment among genome segments
during coinfection of ticks or vertebrates seems likely to have played a
role in generating diversity in this virus.
Based on the sequence data, seven genotypes of CCHFV have been
recognised: Africa 1 (Senegal), Africa 2 (Democratic Republic of the
Congo and South Africa), Africa 3 (southern and western Africa), Europe
1 (Albania, Bulgaria, Kosovo, Russia and Turkey), Europe 2 (Greece),
Asia 1 (the Middle East, Iran and Pakistan) and Asia
2(China, Kazakhstan, Tajikistan and Uzbekistan).
28

29. 29

30. Outbreaks in the world
From 1995 to 2013, 228 cases of CCHF were reported in the
Republic of Kosovo, with a case-fatality rate of 25.5%.
Between 2002–2008 the Ministry of Health of Turkey reported
3,128 CCHF cases, with a 5% death rate. In July 2005,
authorities reported 41 cases of CCHF in central
Turkey's Yozgat Province, with one death. As of August 2008, a
total of 50 deaths were reported for the year thus far in various
cities in Turkey due to CCHF.
In September 2010, an outbreak was reported in
Pakistan's Khyber Pakhtunkhwa province. Poor diagnosis and
record keeping caused the extent of the outbreak to be
uncertain, though some reports indicated over 100 cases, with
a case-fatality rate above 10%.
30

31. In January 2011, the first human cases of CCHF in India
was reported in Sanand, Gujarat, India, with 4 reported
deaths, which included the index patient, treating physician
and nurse.
As of May 2012, 71 people were reported to have
contracted the disease in Iran, resulting in 8 fatalities.
In October 2012, a British man died from the disease at
the Royal Free Hospital in London. He had earlier been
admitted to Gartnavel General Hospital in Glasgow, after
returning on a flight from Kabul in Afghanistan.
In July 2013, seven persons died due to CCHF in Kariyana
village in Babra taluka, Amreli district, Gujarat, India.
31

32. In August 2013, a farmer from Agago, Uganda was
treated at Kalongo Hospital for a confirmed CCHF
infection. The deaths of three other individuals in
the northern region were suspected to have been
caused by the virus. Another unrelated CCHF
patient was admitted to Mulago Hospital on the
same day. The Ministry of Health announced on the
19th that the outbreak was under control, but the
second patient, a 27-year-old woman
from Nansana, died on the 21st. She is believed to
have contracted the virus from her husband, who
returned to Kampala after being treated for CCHF
in Juba, South Sudan.
32

33. In June 2014, cases were diagnosed in Kazakhstan. Ten
people, including an ambulance crew, were admitted on to
hospital in southern Kazakhstan with suspected CCHF.
In July 2014 an 8th person was found to be infected with
CCHF at Hayatabad Medical Complex (HMC), Pakistan.
The eight patients, including a nurse and 6 Afghan
nationals, died between April and July 2014.
As of 2015, sporadic confirmed cases have been reported
from Bhuj, Amreli, Sanand, ar and Vadnagar in Gujarat,
India. In November 2014, a doctor and a laborer in north
Gujarat tested positive for the disease. In the following
weeks, three more people died from CCHF
33

34. In March 2015, one more person died of CCHF in
Gujarat. As of 2015, among livestock, CCHF was
recognized as "widespread" in India, only 4 years after the
first human case had been diagnosed.
In August 2016, the first local case of CCHF in Western
Europe occurred in Western Spain. A 62-year-old man,
who had been bitten by a tick in Spain died on August 25,
having infected a nurse. The tick bite occurred in
the province of Ávila, 300 km away from the province of
Cáceres, where CCHF viral RNA from ticks was amplified
in 2010. As of July 2017 it was unclear what specific
ecology led to the Spanish cases
34

35. In August 2016, a number of Pakistani news sources
raised concerns regarding the disease. Between
January and October 2016, CCHF outbreaks in
Pakistan were reported with highest numbers of cases
and deaths during August 2016, just before the festival
of Eid-al-Adha (held on September 13–15 in 2016). It
was hypothesized that the festival could play an
important part as people could come into contact with
domestic or imported animals potentially infected with
CCHF virus. The Pakistani NIH showed there was no
correlation, and that CCHF cases have coincided with
the peak tick proliferation during the preceding 8–10
years
35

36. In 2017, the General Directorate of Public Health in Turkey,
published official records of infections and casualties of
Crimean Congo Hemorrhagic Fever seen between 2008-
2017. Hundreds of cases were observed each year with
the lowest being 343 in 2017, and the highest being 1318
in 2009 whereas the mortality rate per population
decreasing consistently each year. Geographically cases
are concentrated in the Central Black Sea Region, mostly
in Yozgat Province and surrounding provinces,
mountainous parts of Central Anatolia, and northern
provinces of Eastern Anatolia.
On February 5, 2020, an outbreak occurred in the central
region of Mali. The infected are from Douentza and Mopti
region. So far 7 people have died
36

37. In Iraq, the Crimean-Congo Hemorrhagic Fever was
unknown till September 1979, when a 24 years old lady
was admitted to ALyarmok hospital in Baghdad with
bleeding tendency on the 7th of Sep.1979, and after 2
days, she died. After 4 days, the physician and one of
the health workers who were in close contact with the
patient developed fever, headache, and bleeding from
gastrointestinal tract. Unfortunately, they died too.
During that same year, 10 cases were reported (8 were
female and 2 were male) also; and seven out of ten
died. All the cases were in contact with animal except
the physician and the health worker (Tantawi HH, 1980;
Emad S. et al., 2012) .
37

38. In Iraq:
Crimean –Congo Hemorrhagic Fever
Between Sept. and Nov./1979 , 925 randomly selected persons living
in different areas were checked for serological evidence of C.C.H.F.
4.54 % were positive (17) .In experimental infection virus appear in
the blood stream in 1 – 5 days of inoculation, three isolates had been
recovered from sheep in patients houses and two isolates from adult
ticks of Hyalomma marginatum in Aziziya district (18). Other study a
total of 551 persons and 270 farm animals ( 93 sheep, 93 cow , 84
goat) and 50 rat were examined for the detection of CCHF-IgG in a
focus in Diyala Governorates the prevalence of positive sera was 6.4%
in persons and 33.3% in cow and sheep and 28.5 in goat
respectively(19,20) .Nosocomial infection in Iraq were reported three
times at 1979 (2 cases were died ) , 1992 (2 cases) , and 1996 (1case)
(17,21). There are about 192 confirmed cases of CCHF have been
reported from different provinces of Iraq (between 1992 and Dec.
2010); however, five cases of nosocomial infections were recorded in
1979, 1992 and 1996(17,
21)
38

39. The total number of suspected cases was 143 cases. Most
of the cases were males (59.4%), 15-45 years old (62.2%),
and live in urban areas (58.7%). About three quarters of
the cases (68.5%) did not fit the standard case definition
adopted by Iraq CDC. Most of the suspected cases were
reported in Diwaniya province (20.3%). Nearly half of the
suspected cases (64, 44.7%) occurred in June. Only 7.0%
of the total suspected cases were positive when tested by
Reverse Transcriptase Polymerase Chain Reaction (RT-
PCR). The majority of confirmed cases (3, 30.0%) occurred
in Diwaniya province(Mustafa, 2018)
39

40. 40
Crimean-Congo Hemorrhagic Fever - Iraq
Outbreak at a glance
Between 1 January to 22 May 2022, the health authorities
of the Republic of Iraq notified WHO of 212 cases of
Crimean-Congo Hemorrhagic Fever (CCHF), of which 115
(54%) were suspected and 97 (46%) laboratory-confirmed;
there were 27 deaths, 14 in suspected cases and 13 in
laboratory confirmed cases. The number of cases reported
in the first five months of 2022 is much higher than that
reported in 2021, when 33 laboratory confirmed cases
were recorded. Cases have been reported in several areas
(governorates) in Iraq and the outbreak may pose
additional pressure to an already over-stretched health
care system.

41. 41

42. 42
•
To date11 August , 1085 suspected Crimean Congo
Hemorrhagic Fever cases were reported, of which
287 were confirmed by laboratory, with 83 related
suspected deaths and 52 deaths among confirmed
cases (representing 18.1% of case fatality rate). All
governorates reported confirmed cases, except for
Sulaymaniyah.
•ON 18 August 295 lab-confirmed cases of Crimean
Congo Hemorrhagic Fever (CCHF) reported

43. Diagnosis
CCHF virus infection can be diagnosed by several different laboratory
tests:
•enzyme-linked immunosorbent assay (ELISA) ;
•antigen detection;
•serum neutralization;
•reverse transcriptase polymerase chain reaction (RT-PCR) assay;
and
•virus isolation by cell culture.
Patients with fatal disease, as well as in patients in the first few days
of illness, do not usually develop a measurable antibody response
and so diagnosis in these individuals is achieved by virus or RNA
detection in blood or tissue samples.
Tests on patient samples present an extreme biohazard risk and
should only be conducted under maximum biological containment
conditions. However, if samples have been inactivated (e.g. with
virucides, gamma rays, formaldehyde, heat, etc.), they can be
manipulated in a basic biosafety environment.
43

44. 44
conventional PCR performed only on positive samples
obtained from real-time PCR. CCHFV small (S) segment
(encoding for the nucleocapsid protein) specific primer
pairs (F3: 3′-GAATGTGCATGGGTTAGCTC-5′ and R2: 3′-
GACATCACAATTTCACCAGG-5′) and same PCR conditions
defined by Schwarz et al. (7) were used in the PCR.
Sequence analysis was performed on the ≈260-bp PCR
product, when positivity was detected, by using the
primers of F3 and R2 in the ABI 310 Genetic Analyzer
(Applied Biosystems, Foster City, CA,
USA)

45. Treatment and control
General supportive care with treatment of symptoms is the main approach to
managing CCHF in people.
The antiviral drug ribavirin has been used to treat CCHF infection with apparent
benefit. Both oral and intravenous formulations seem to be effective.
•Reducing the risk of tick-to-human transmission:
• wear protective clothing (long sleeves, long trousers);
• wear light coloured clothing to allow easy detection of ticks on the clothes;
• use approved acaricides (chemicals intended to kill ticks) on clothing;
• use approved repellent on the skin and clothing;
• regularly examine clothing and skin for ticks; if found, remove them safely;
• seek to eliminate or control tick infestations on animals or in stables and barns;
and
• avoid areas where ticks are abundant and seasons when they are most active.
•Reducing the risk of animal-to-human transmission:
• wear gloves and other protective clothing while handling animals or their tissues
in endemic areas, notably during slaughtering, butchering and culling procedures
in slaughterhouses or at home;
• quarantine animals before they enter slaughterhouses or routinely treat animals
with pesticides two weeks prior to slaughter.
•Reducing the risk of human-to-human transmission in the community:
• avoid close physical contact with CCHF-infected people;
• wear gloves and protective equipment when taking care of ill people;
• wash hands regularly after caring for or visiting ill people.
45

46. Controlling infection in health-care settings
Health-care workers caring for patients with suspected or
confirmed CCHF, or handling specimens from them, should
implement standard infection control precautions. These
include basic hand hygiene, use of personal protective
equipment, safe injection practices and safe burial practices.
As a precautionary measure, health-care workers caring for
patients immediately outside the CCHF outbreak area should
also implement standard infection control precautions.
Samples taken from people with suspected CCHF should be
handled by trained staff working in suitably equipped
laboratories.
Recommendations for infection control while providing care
to patients with suspected or confirmed Crimean-Congo
haemorrhagic fever should follow those developed by WHO
for Ebola and Marburg haemorrhagic fever.
46

47. 47
Disinfection CCHFV can be inactivated by many disinfectants
including 1% hypochlorite, 70% alcohol, hydrogen peroxide, peracetic
acid, iodophors, glutaraldehyde and formalin. It can also be
destroyed by UV light or pH < 6. One study found that heating at 56°C
(133°F) for 30 minutes inactivated the virus, while another reported
that 60°C (140°F) for 60 minutes was more effective. A recent report
indicated that CCHFV in culture fluid was no longer infectious after 15
minutes at either 56°C or 60°C. CCHFV can survive for a short time in
the environment, especially in some organic material. Infectious virus
was found for up to 10 days, and occasionally longer, in blood kept at
4°C (39°F). Viral RNA was detected for as long as 30 days in serum at
4°C, but infectivity was not assessed in this study. CCHFV was also
reported to remain infectious in serum for at least a few days at
unspecified ambient temperatures, and to be stable “under wet
conditions” for 15 days at 4°C, 11 days at 20°C (68°F) and 7 hours at
37°C (99°F). Dried virus was found to remain infectious for less than
24 hours.

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