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crimean - congo hemorrhagic fever ( cchf ) is an acute tick - borne viral disease caused by cchf virus , a nairovirus genus member of bunyaviridae family .
humans appear to be the only hosts where crimean - congo hemorrhagic fever virus ( cchfv ) produces a severe hemorrhagic disease with a mortality rate up to 30% .
cchf is mainly spread via hyalomma genus ticks and direct contact with blood and tissues of infected persons and viremic animals .
kosova is a frequently affected cchf country with the first reported case in 1954 . since
the genome of kosova 's authentic cchf virus strain kosova - hoti has been completely sequenced revealing characteristic nucleotide sequences especially in the l segment of the genome that may explain its high pathogenicity and mortality .
incubation , prehemorrhagic , hemorrhagic and convalescence phases characterize cchf . the pre - hemorrhagic phase is characterized by fever , chills , headache , muscle pain , dizziness , nausea , vomiting , and diarrhea .
the hemorrhagic phase follows with petechiae , echymosis , gingival bleeding , epistaxis , hematemesis , melena and visceral bleedings .
fatal outcomes of cchf can occur in hemorrhagic phase because of cerebral hemorrhage , severe anemia , hemorrhagic shock , multiple organ failure and coma . an atypical manifestation of cchf was found in an adolescent patient in the form of acute arthritis .
here we report a case of a 15-year - old boy who comes from a rural area known to be a natural cchf focus and presents with fever ( 40c ) , fatigue , anorexia , myalgia , polyarthralgia , backache , 2 days after his brother 's illness .
he denies any tick bite , but admits that he was taking care of his sick brother who first became ill . on day 1 of disease
, he was hospitalized in a regional hospital with the diagnosis of acute febrile illness . on day 3 ,
as his condition was not improving , he is transferred in university clinical center in prishtina as his ill brother tested cchfv positive . in admission
the blood was drawn for laboratory investigations and the measured parameters were as following : e0 rythrocyte count of 4.0  10 cells / mm ; hemoglobin level of 11.0 g / dl ; leukocyte count of 2.0  10/mm ; thrombocyte count of 28  10/mm ; liver enzyme levels : aspartate aminotransferase-377.5 u / l , alanine aminotransferase-154 u / l , lactate dehydrogenase-1558 u / l , creatine phosphokinase-2380
/ l ; fibrinogen-3.2 g / l ; rheumatoid factor - negative ; serum antistreptolysin o antibody titer- 132 units / ml ; blood cultures - negative .
blood real - time - polymerase chain reaction ( rt - pcr ) on day 3 resulted positive for cchfv . on day 4 ,
, his condition deteriorated further with massive bleedings - epistaxis , melena , spontaneous bleeding from injection sites ; hypotension , bradycardia . on abdominal ultrasound hepatosplenomegaly ,
his temperature marked 39c , his clinical condition was severely affected with intense chest pain and muscle aches .
chest x - ray showed right lower lobe infiltrations ; chest computed tomography - scan revealed right lower lobe pleuropneumonia with abscess tendency formation [ figure 2 ] . on day 9 , urine rt - pcr was positive for cchfv . on day 12 ,
patient complained of pain on his left knee , upon examination swelling and limited joint movements were noted .
a left knee x - ray was ordered , orthopedic surgeon was consulted and in the meantime brucellosis , leptospirosis , hepatitis a , b , c and post - streptococcal arthritis were serologically ruled out .
synovial membrane hypertrophy with joint effusion in the level of suprapatellar recess was noted on left knee ultrasound [ figure 3 ] .
after day 16 , knee pain and other signs of inflammation regressed gradually . from day 22
abdominal ultrasound : ( a ) enlarged liver ; disseminated anechogenic nodules implying punctiform bleeding are present ; ( b ) slightly enlarged spleen ; ( c ) gallbladder has edematous walls , an intraluminal anechogenic zone ( liquid - blood ) and pericholecystic fluid ; ( d ) fluid in pleural cavity and abdominal cavity - pleural effusion and hemoperitoneum diagnostic testing for chest pain : ( a ) chest - x - ray showing right lower lobe infiltration ; ( b ) chest computed tomography ( ct ) scan shows right lower lobe pleuropneumonia with abscess tendency formation ; ( c ) chest ct scan evidencing pleural effusion left knee joint : ( a ) marked swelling is noted ; ( b ) left knee x - ray : anterior - posterior and lateral views , soft - tissue swelling above and below patella is noted , synovitis was suggested ; ( c ) and ( c ' ) left knee ultrasound : synovial membrane hypertrophy and joint effusion are noted
nevertheless , endothelial cells , immune mechanisms , viral load and coagulation cascade are implicated in its pathogenesis .
viral replication takes place in endothelial cells , followed by cd4 + t - helper cell activation that by secreting enormous amounts of tumor necrosis factor ( tnf ) , il-1 , il-6 causes macrophage co - activation . both viral replication and massive cytokines release damage the endothelium of blood vessels promoting vasodilatation , platelet aggregation and activation of coagulation cascade , hemorrhage , disseminated intravascular coagulation and multi - organ failure .
activated macrophages can lead to hemophagocytosis syndrome , where macrophages phagocytize blood cells causing the characteristic cytopenia encountered in cchf .
a study by ergonul et al . found increased levels of tnf , il-1 and il-6 in cchf patients , supporting the crucial role of cytokines in cchf pathogenesis .
viruses are a known cause of arthritis and arthralgias and how they elicit arthritis depends both on host and viral factors
. viruses mainly initiate rheumatic symptoms by direct invasion of synovium or by deposition of immune complexes into joint spaces .
patients present with symmetric polyarticular arthralgias or arthritis that can be associated by a rash , which generally occurs before or with the clinical onset of infection . considering cchf mechanisms of disease development such as endothelial viral replication , intense activation of macrophages and massive cytokine release it can be thought that the same may apply to the arthritic symptoms encountered in cchf associated arthritis , as activated synovial macrophages can make joint inflammation unavoidable .
immune mediated mechanisms in the pathogenesis of cchf associated acute arthritis can not be excluded .
however , the involvement of a single large joint and the development of acute arthritis later in disease course imply that arthritic symptoms may be a consequence of bleeding disorder underlying cchf .
acute arthritis might be a part of hemorrhagic syndrome present in cchf virus infection , even though its manifestation through monoarticular joint swelling and pain does not belong to the cchf characteristic clinical picture .
affected joint with acute hemarthrosis is swollen , warm , painful with reduced range of motion and usually only one joint is affected at a time which can explain our patient 's knee symptoms .
synovial hypertrophy [ figure 3 ] is a known early consequence of toxic effects of blood products and if inflammation is ongoing fibrosis and impaired joint movement may result .
our patient recovered fully from acute arthritis regardless of possible mechanisms that led to its development .
crimean - congo hemorrhagic fever is a severe viral disease caused by a nairovirus . 
 an atypical manifestation in the form of acute arthritis was found in a confirmed crimean - congo hemorrhagic fever virus kosova - hoti strain positive patient . 
 acute arthritis in crimean - congo hemorrhagic fever ( cchf ) may be as a result of immune mechanisms or the bleeding disorder underlying cchf .