Q FEVER

Q fever is a zoonotic disease with an almost worldwide distribution – it is only absent from Antarctica and New Zealand [10].

C. burnetii is a gram-negative rod bacterium.

It is a strictly intracellular bacterium, with the mammalian host cell being the macrophage [10]. Within macrophages, C. burnetii multiples in the phagolysosome [3], allowing evasion of the hosts immune system.

Causative Agent: Coxiella burnetii

SOURCES OF INFECTION

Q fever has a wide reservoir of potentially infective species, including [11]:

Ruminants - cattle, sheep, goats
Dogs
Cats
Rabbits
Wildlife (e.g. kangaroos)

Ruminants are the primary reservoirs responsible for the infection of humans with C. burnetii, with the bacteria being shed during birthing through the placenta and amniotic fluids [11].

PATHOGENESIS

Source: Veterian Key, 2016, Coxiellosis and Q fever, viewed 26 October 2018, <https://veteriankey.com/coxiellosis-and-q-fever/>

Source of Infection

Pathogenesis

The pathogen is highly resilient in the environment, remaining infective in aerosols for up to 2 weeks and in soil for 5 months [12].

C. burnetii gains entry into humans through the oropharynx via aerosolisation or ingestion [12]. The infectious dose can be as little as one organism and the incubation time varies from 2-4 weeks [13].

The organism replicates in the regional lymph nodes before localizing in the mammary glands and placenta of pregnant females. Furthermore, the bacteria can spread within the body via blood, resulting in liver, spleen, bone marrow and reproductive tract infection [12]. C. burnetii may persist after acute or subacute disease, before being shed when an infected female falls pregnant [12].

DISEASE MANIFESTATION

Clinical Signs

ACUTE PHASE DISEASE

Begins 2-3 weeks after initial exposure

40% of patients become symptomatic at the acute stage of Q-fever infection [5,6,14]. They exhibit flu-like symptoms such as:

Fever
Chills
Tremors
Headaches
Drenching sweats
Muscle and joints pains
Extreme fatigue

2-5% of infected people develop severe physiological complications that may lead to hospitalisation, such as [5]:

Hepatitis
Pneumonia
Myocarditis
Meningitis

1% of acute Q Fever infections in humans are fatal [6].

DIAGNOSIS

Reliable diagnosis of Q fever is achieved through measuring antibodies your body produces in fighting the bacteria.

Laboratory Pathology Protocol [15]

Two blood samples are taken three weeks apart
Two samples are required because you might have been previously exposed to this disease and then cleared it, and as such still have the antibodies
An increase in antibody levels would indicate that you are currently infected with C. burnetti.

Additional Tests [15]

Supplementary diagnostic tests include growing bacteria and detecting DNA. These tests must be used in conjunction with antibody tests to ensure the diagnosis in fact accurate.

Diagnosis

TREATMENT

Treatment

In some cases, people recover with little to no treatment after a period of short illness. When this does not occur, the following treatment may be provided:

Acute Phase Disease

The first line treatment is tetracyclines, most commonly doxycycline, in combination with an alkalizing agent such as hydroxychloroquine. The alkalizing agent is used to produce an alkaline environment within the phagolysosome in which C. burnetti is replicating, thereby allowing the doxycycline to become bactericidal [16].

Both components of this treatment can cause toxicity. As such, co-trimoxazole is used for pregnant women to reduce the risk of miscarriage and young children [17].

Chronic Phase Disease

The first line treatment is an extended course of doxycycline and hydroxychloroquine for 18 months minimum [18].

A study by Keijmel et al. (2017) investigated a cognitive behavioural therapy with a step-wise increase in physical activity and challenging dysfunctional fatigue-related beliefs. It was found to be effective in reducing fatigue severity and the level of psychological distress when compared to a placebo (control).