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Q Fever

Updated : June 23, 2022





Background

Australia was the first country where Q fever, and acute zoonotic febrile sickness, was identified in meat employees in 1935. It was classified as “Q (question) fever” because no cause could be found.

Farm workers who handle ungulates and animals have both contracted this disease in outbreaks. Although severe signs can happen, the clinical presentation is frequently a self-limited febrile sickness.

Epidemiology

Because it might be used as a bioweapon, Q fever has become a sickness that Americans must report since 1999. It is an illness that is both underdiagnosed and underreported. Three to one is the male to female ratio. The positive seropositivity rate in Americans is 3.1 percent, and it is more prevalent in men, the elderly, Hispanics, and the poor. Coxiella is carried by soft ticks and certain other arthropods, which transmit the disease to both wild and domestic animals through bites or contact with contaminated host skin.

Domestic cows, goats, and sheep are the most prevalent reservoirs, preceded by camels, horses, pigs, dogs, turkeys, ducks, and pigeons. Other animals that can act as reservoirs include squirrels, wild birds, rabbits, mice, rats, and cats. Despite the fact that Q fever can strike anywhere at any time of each year, the majority of cases happen in the early summer (April or May) and spring, when calves, goats, and sheep are giving birth.

Coxiella is highly concentrated in the milk, urine, placenta, and feces of infected animals; as a result, those who handle infected laundry, consume infected unpasteurized milk, are exposed to the placenta of infected animals, or get viable cell treatment using reprocessed animal fetal cells are all at risk for infection. Therefore, it is a condition that affects those who work with animals on a regular basis, such as farmers, veterinary professionals, and people who work in slaughterhouses.

The disease can also be spread indirectly through aerosols from contaminated straw, manure, and farm vehicle dust. Additionally, transmission to people can happen through blood donations, autopsy, clinical care (delivery of pregnant patients with the infection), removing contaminated devices, and consuming raw milk.

Recent epidemics in European nations were brought on by urban goat and sheep rearing, and people who lived close to the sheep farms were more likely to be attacked. The recent breakouts in the Netherlands from 2007 to 2010 were caused by urbanized goat farming. Severe symptoms are more likely to occur in HIV-positive as well as other immunosuppressed patients.

Anatomy

Pathophysiology

The most likely means of transmission are aerosols inhaled from an infected animal placenta after parturition, dust, animal waste, or straw from a farm vehicle or farm. Another possible mechanism of transmission in humans is via the digestive system. Acute Q fever typically takes 20 days to incubate. In the event of bacteremia, which develops as a result of aspirated Coxiella bacteria multiplying in the airways, systemic symptoms appear.

The severity of a disease is determined by the virus replication of the strain of bacteria and the dose that causes infection; for example, the strains that include the QPH1 and QPRS plasmids are much more aggressive than the others. Primary infection can either be symptomatic (Q fever) or symptomless depending on the host’s immunological response. Based on the host, either or both can develop into endocarditis.

The likelihood of remaining asymptomatic is higher in women and children, which include pregnant women. Despite being asymptomatic, endocarditis is more likely to affect pregnant women, and those with valvular heart disease, cancer, or arterial aneurysms. Anticardiolipin IgG antibodies and elevated IL-10 are linked to endocarditis. An abnormal immunological response brought on by a persistent infection may account for QFFS (Q fever exhaustion syndrome).

Etiology

Genetics

Prognostic Factors

When identified and managed as soon as possible, acute Q fever has a very good prognosis. Endocarditis is a danger for patients with established valvular heart disease as well as pregnant women who have acute Q fever.

For patients with increased serologic titers, routine serology monitoring and echocardiography are advised. Treatment for Q fever during pregnancy frequently yields better results. Dual therapy is more effective than monotherapy in treating endocarditis.

Clinical History

Physical Examination

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Differential Diagnoses

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

Medication

 

clarithromycin 

Acute symptomatic:

500 mg oral tablet immediate release twice a day for 14 days



 
 

Media Gallary

References

https://www.ncbi.nlm.nih.gov/books/NBK556095/

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Q Fever

Updated : June 23, 2022




Australia was the first country where Q fever, and acute zoonotic febrile sickness, was identified in meat employees in 1935. It was classified as “Q (question) fever” because no cause could be found.

Farm workers who handle ungulates and animals have both contracted this disease in outbreaks. Although severe signs can happen, the clinical presentation is frequently a self-limited febrile sickness.

Because it might be used as a bioweapon, Q fever has become a sickness that Americans must report since 1999. It is an illness that is both underdiagnosed and underreported. Three to one is the male to female ratio. The positive seropositivity rate in Americans is 3.1 percent, and it is more prevalent in men, the elderly, Hispanics, and the poor. Coxiella is carried by soft ticks and certain other arthropods, which transmit the disease to both wild and domestic animals through bites or contact with contaminated host skin.

Domestic cows, goats, and sheep are the most prevalent reservoirs, preceded by camels, horses, pigs, dogs, turkeys, ducks, and pigeons. Other animals that can act as reservoirs include squirrels, wild birds, rabbits, mice, rats, and cats. Despite the fact that Q fever can strike anywhere at any time of each year, the majority of cases happen in the early summer (April or May) and spring, when calves, goats, and sheep are giving birth.

Coxiella is highly concentrated in the milk, urine, placenta, and feces of infected animals; as a result, those who handle infected laundry, consume infected unpasteurized milk, are exposed to the placenta of infected animals, or get viable cell treatment using reprocessed animal fetal cells are all at risk for infection. Therefore, it is a condition that affects those who work with animals on a regular basis, such as farmers, veterinary professionals, and people who work in slaughterhouses.

The disease can also be spread indirectly through aerosols from contaminated straw, manure, and farm vehicle dust. Additionally, transmission to people can happen through blood donations, autopsy, clinical care (delivery of pregnant patients with the infection), removing contaminated devices, and consuming raw milk.

Recent epidemics in European nations were brought on by urban goat and sheep rearing, and people who lived close to the sheep farms were more likely to be attacked. The recent breakouts in the Netherlands from 2007 to 2010 were caused by urbanized goat farming. Severe symptoms are more likely to occur in HIV-positive as well as other immunosuppressed patients.

The most likely means of transmission are aerosols inhaled from an infected animal placenta after parturition, dust, animal waste, or straw from a farm vehicle or farm. Another possible mechanism of transmission in humans is via the digestive system. Acute Q fever typically takes 20 days to incubate. In the event of bacteremia, which develops as a result of aspirated Coxiella bacteria multiplying in the airways, systemic symptoms appear.

The severity of a disease is determined by the virus replication of the strain of bacteria and the dose that causes infection; for example, the strains that include the QPH1 and QPRS plasmids are much more aggressive than the others. Primary infection can either be symptomatic (Q fever) or symptomless depending on the host’s immunological response. Based on the host, either or both can develop into endocarditis.

The likelihood of remaining asymptomatic is higher in women and children, which include pregnant women. Despite being asymptomatic, endocarditis is more likely to affect pregnant women, and those with valvular heart disease, cancer, or arterial aneurysms. Anticardiolipin IgG antibodies and elevated IL-10 are linked to endocarditis. An abnormal immunological response brought on by a persistent infection may account for QFFS (Q fever exhaustion syndrome).

When identified and managed as soon as possible, acute Q fever has a very good prognosis. Endocarditis is a danger for patients with established valvular heart disease as well as pregnant women who have acute Q fever.

For patients with increased serologic titers, routine serology monitoring and echocardiography are advised. Treatment for Q fever during pregnancy frequently yields better results. Dual therapy is more effective than monotherapy in treating endocarditis.

clarithromycin 

Acute symptomatic:

500 mg oral tablet immediate release twice a day for 14 days



https://www.ncbi.nlm.nih.gov/books/NBK556095/

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