VIRAL HAEMORRHAGIC FEVERS / MedUrgent


VIRAL HAEMORRHAGIC FEVERS




Viral Hemorrhagic Fever defines a syndrome caused by 4 different families of RNA viruses. Though they have constant features in common, yet there are particular clinical features associated with different viruses. They can cause disastrous epidemics with case fatality rate up to 50%.

Classification

1. Arenaviruses e.g. Guanarito, Junin, Machupo and Lassa. They have rodent reservoir. Humans are infected by aerosols of rodent excreta or other close contacts with rodents.

2. Bunyaviruses e.g. Rift Valley, Criean-Congo and Hantaan. Transmission through mosquito bites, aerosols or contact with blood of domestic animals, tick bite and rodent excreta.

3. Filovirus e.g. Ebola and Marburg. Mode of transmission is by person to person through body fluids

4. Flaviviruses e.g. yellow fever, Dengue and Kyanasur forest disease. Mode of transmission is through mosquito and tick bites. 


Clinical features

After contracting the disease, the incubation period is 2 days to 3 weeks in average. VHF presents with fever, myalgia and malaise for a few days and then the disease progresses with increased prostration and specific organ involvement. Bleeding, jaundice, anuria, oedema, conjunctival and retinal hemorrhages, CNS involvement. Shock and coma are common terminal events.


Laboratory tests

Virology studies need highly equipped laboratories. WHO should be informed in suspicious cases or epidemics.


Management

• Supportive therapy

• Ribavirin when administered early is effective in reducing mortality rate in cases of Lassa fever, Crimean-Congo fever, Arena virus, Rift Valley fever and HF with renal syndrome.



DENGUE HAEMORRHAGIC FEVER

Dengue fever is caused by an arbovirus transmitted to man by the daybiting Aedes mosquito. It has 4 serotypes (1, 2, 3, and 4) and there is no cross-immunity to these serotypes. Almost all infections occur in children as adults are usually immune to the locally circulating serotype of dengue virus.





Clinical Features

The disease starts apruptly 3–15 days after a mosquito bite and presents as either:

1. Undifferentiated febrile disease with severe headache, retro-orbital pain, blanching maculopapular rash, arthalgia, and myalgia and may progress to encephalopathy.

2. A febrile illness with bleeding and shock.


WHO CASE DEFINITION OF DENGUE HAEMORRHORRAGIC FEVER

All these features must be present:

A. Fever                                         

B. Hemorrhagic tendency:

at least one of the following:

i) Positive tourniquet test

II) Petechiae, purpura or ecchymosis

III) Bleeding

C. Thrombocytopenia

D. Evidence of plasma leakage:

i) Haematocrit>20% above average

II) Drop in haematocrit > 20% after volume replacement

III) Clinical signs e.g. pleural effusion and ascites.

 

WHO DEFINITION OF DENGUE SHOCK SYNDROME 

All features of DHF plus evidence of circulatory failure:

a) Rapid and weak pulse

b) Narrow pulse pressure <20mm Hg

OR

a) Hypotension

b) Cold clammy skin and restlessness. 


Laboratory tests

a) PCR

b) Immunocytochemistry

c) Antibodies: IgM (acute phase), IgG (rising titre) 

d) Virus Culture.


Treatment

• No specific antiviral drug

• Conservative therapy

• IV fluids; Ringer lactate or colloids to restore plasma losses.

• Blood transfusion


 

YELLOW FEVER


Yellow fever is caused by a flavivirus which is transmitted by culicine mosquito. It causes explosive epidemics.

Clinical features

The disease starts abruptly 3-6 days after a mosquito bite with fever, chills, headache, myalgia, conjunctival congestion and relative bradycardia (Faget's sign). Jaundice, renal failure, bleeding, shock, coma and death may follow.

Treatment

• Supportive therapy. No specific treatment.




Ebola Hemorrhagic Fever 

(Ebola Virus Disease)

 The name Ebola is derived from a river in Congo (Zaire) where the first epidemic reported in a village near this river in 1976. The disease is caused by a Cilovirus called Ebolavirus that has 6 known species. Central and West Africa are the mostly affected areas. The vector is the fruit bat that spreads the virus through it's saliva and excreta, there for mostly affected people are forest workers and miners. Nosocomial spread may occur where preventive measures and precautions are not followed properly. Monkeys are similarly affected and can act as an intermediate host. Epidemics occur usually at the end of the rainy seasons.







Clinical Features

The virus is usually disseminated to all organs causing necrosis and leading to a severe disease, though asymptomatic cases have been reported. It starts as fever, fleeting maculopapular rash on the face, abdominal pain due to the enlarging tender liver. Severe bleedings and renal failure are signs of end-stage disease. Complications include jaundice, hair loss, infection of testes and semen, eye infection and hemorrhage, delirium, seizures and coma.

Laboratory diagnosis

-PCR

-ELISA

-Culture

Treatment

-There is no specific treatment

- Supportive therapy

-Monoclonal antibody therapy is on trial now

 

Prevention and Control

- Vaccination

- Avoid the habitat of bats e.g. dense forests, mines, caves...etc

- Avoid eating of monkey meat or exposure to it's blood or body fluids.


Chikungunya

 Chikungunya is a Tanzanian word meaning "bends up". The disease is caused by an Arbovirus (CHKV) which is widely spread in Africa, India, Saudi Arabia, South East Asia and the islands of South West Indian Ocean. The vectors are Aedes egypti and Aedes albopictus. It affects humans, monkeys and baboons and appears usually in an epidemic form. Clinical Features Incubation period is 3 – 12 days . Epidemics occur mainly during wet seasons. It presents with fever and arthralgia which is usually symmetrical, affecting the small joints and may persist for months or years. Other features include severe back pain, generalized maculopapular rash, conjunctivitis and photophobia, mild hemorrhagic episodes especially in children, chills, nausea and vomiting. It is usually a self-limiting disease with a low fatality rate; however, complications do occur e.g. myocarditis and meningoencephalitis.

Laboratory diagnosis

- PCR

- High IgM

- Rising Hl or N antibody titer

- Culture

Treatment

- No specific treatment

- General symptomatic treatment

- Hydroxychloroquin for arthritis.



RELAPSING FEVERS

Relapsing fevers are caused by Borrelia spirochetes. The disease, if untreated, relapses repeatedly between afebrile intervals of 5-9 days. Borrelia recurrentis causes epidemics and it is transmitted by the human body lice pediculus humanous. Endemic Relapsing Fever is caused by other species of borrelia that are transmitted by ticks. 

Clinical features

The incubation period is 4-17 days. Realpsing fever starts with sudden high grade fever followed by headache, confusion, myalgia, arthralgia, nightmares and prostration, bleedings, jaundice, chest signs and hepatosplenomegaly. During pregnancy, the disease may lead to abortion.

This phase ends with an afebrile period of 5-9 days, then, if untreated, it relapses. Death may occur due to myocarditis, liver failure, severe bleeding, DIC, rupture of the spleen or secondary bacterial infections. During epidemics Case Fatality Rate is 40%  or even more.

Laboratory tests

- Blood film stained with Gimsa stain to see the spirochetes.

- Full blood count shows pancytopoenia

Treatment

• A single dose of antibiotic is curative (tetracycline, benzyl penicillin, erythromycin or chloramphenicol).

• General supportive measures.

 

Jarisch-Hexheimer Reaction

This syndrome occurs a few hours after treatment of Relapsing Fever. It manifests as restlessness, high grade fever, rigors, delirium, cough, diarrhea and vomiting, profuse sweating, shock and pulmonary oedema secondary to myocarditis. Death rate is high if untreated. Treatment includes cooling of temperature, circulatory support and digoxine.

Comments

Popular posts from this blog

Management of Severe Malnutrition / MedUrgent

TETANUS / MedUrgent