This was a rare case of primary
T. gondii infection in an AIDS patient with HPS who previously experienced virological and immunological failure and had not been administered primary prophylaxis with SMZ-TMP. We were unable to find any published reports of primary
T. gondii infection with HPS in patients with HIV. The primary
T. gondii infection was initially identified based on the seroconversion from single-positive IgM antibody to double-positive IgM and IgG antibodies. However, the sensitivity, specificity and positive predictive values of IgM antibody by enzyme-linked immune sorbent assay for acute toxoplasmosis infection have been reported to be 98.1%, 65.0% and 43.3%, respectively [
5]. False positive
T. gondii IgM antibody can occur due to cross-reactivity with various autoimmune antibodies [
6], while false negative
T. gondii IgG antibody can occur in immune compromised individuals [
7]. The diagnosis of disseminated
T. gondii infection was subsequently confirmed by mNGS of a plasma sample. To our knowledge, only two cases HIV-infected patients with
T. gondii infection-associated HPS have previously been reported, and both were due to reactivated
T. gondii infection with positive IgG and negative IgM antibodies [
8,
9]. Reactivation of latent
T. gondii infection is more common than primary infection in patients with HIV, and most reported cases of primary
T. gondii infection were from kidney transplant recipients [
2]. In HIV-infected individuals, regardless of their immune status, primary
T. gondii infection is generally asymptomatic [
4,
10,
11], although some reported manifestations of macular rash [
12] or acute respiratory distress [
13]. In China the seroprevalence of
T. gondii infection was 8.2% from 2000 to 2007, but has increased in recent years [
14]. The prevalence of
T. gondii IgG antibody in individuals with HIV infection has been reported to be higher than that of healthy controls (9.7% vs. 4.7%), while the seroprevalences of
Toxoplasma IgM antibody is similar in both groups [
15].In this patient, the level of
T. gondii IgM and IgG antibodies increased greatly in the convalescent period. Generally,
T. gondii antibody levels returned to normal within 4–6 months; however, some cases reported persistence of positive
T. gondii IgM longer than 1 year. In this case, the delayed disappearance of
T. gondii IgM antibody may be associated with obvious immune function restoration from HPS and virological control after adjusting the regimen of ART. Notably, serum
T. gondii antibodies were only tested at baseline, 1 week, and at 4 months, possibly missing the peak level of
T. gondii IgM antibody.
The lung is the second most common site of
T. gondii infection. In transplant recipients and individuals with HIV infection, respiratory manifestations of acute toxoplasmosis usually present as a subacute febrile illness with cough and dyspnea. Patients with
T. gondii pneumonia have significantly higher LDH levels than those with PJP. The diagnosis of pulmonary toxoplasmosis is challenging due to the nonspecific nature of clinical and radiographic findings. Chest CT may reveal centrilobular patchy or diffuse ground-glass opacities resembling PJP. Extrapulmonary involvement may be present in the liver, brain, bone marrow, heart, and stomach. Pulmonary coinfection of
T. gondii and
P. jirovecii has been reported [
16]. Although no bronchoalveolar lavage fluid (BALF) specimen was tested in this case, the blood mNGS did not detect
P. jirovecii, suggesting that the patient had
T. gondii monoinfection without
P. jirovecii coinfection.
Among different specimens, hematoxylin and eosin stainings, immunoperoxidase staining, and polymerase chain reaction (PCR) can be used for the detection of
T. gondii. However, PCR detection for
T. gondii was unavailable in our hospital. In this patient, cerebrospinal fluid (CSF), bone marrow specimen, and BALF specimen were not obtained. Patients with TE can be diagnosed by mNGS using CSF specimen [
19]. However, to our knowledge, there have been no previous reports of mNGS being used to diagnose toxoplasmosis using a peripheral blood sample.