Chlamydia psittaci Crosses Into the Central Nervous System in Chile
A confirmed case of Chlamydia psittaci meningitis in a 50-year-old farm worker from southern Chile adds a rare zoonotic diagnosis to the differential for atypical meningitis in Latin America. The infection was established by cerebrospinal fluid quantitative real-time PCR and supported by serology, after routine bacterial, viral, and fungal testing failed to identify a cause. The patient recovered after antimicrobial treatment.
This is not the pattern clinicians expect when they see a febrile farm worker with headache and sore throat. Psittacosis is usually framed as a respiratory illness, yet the organism can invade organs beyond the lungs, including the central nervous system, where it may present as meningitis or encephalitis with few of the bedside clues that usually steer clinicians toward meningeal disease.
A Rural Exposure History Pointed Toward Zoonosis
The patient first sought care on August 14, 2023, at a rural health center with fever above 38°C, myalgia, chills, headache, and painful swallowing. He was diagnosed with tonsillitis and received intramuscular benzathine penicillin. Ten days later, persistent fever and headache led to hospital referral for suspected meningitis.
His occupation mattered. He worked as a tractor operator on a dairy farm and had occasional direct contact with cattle during calving assistance and milking. He also reported an increase in bovine abortions on the farm before illness onset. He denied direct bird contact, but wild parrots and domestic chickens were present on the property. In a zoonotic illness, that kind of environmental detail can be the difference between a routine infectious workup and a targeted search for an uncommon pathogen.
On admission, the patient had an erythematous pharynx but remained alert and oriented. Neurologic examination was reassuring: cranial nerves were intact, motor function and tone were preserved, and no meningeal irritation was present. The absence of classic meningeal signs did not exclude CNS infection, and the laboratory profile still pointed to inflammation: leukocytosis of 11,400/mm3 with 65% neutrophils, C-reactive protein of 16.8 mg/L, and mildly elevated liver enzymes.
Cerebrospinal Fluid Findings Were Inflammatory but Nonspecific
CSF was clear and colorless, yet profoundly abnormal. It contained 1,033 leukocytes/mm3 with a mixed cellular response, 56% mononuclear and 44% polymorphonuclear cells, protein of 1.21 g/L, and glucose of 50.1 mg/dL. Those results established a meningitic process, but they did not identify the organism.
Routine testing came back negative across a broad front. Gram stain and a multiplex meningitis/encephalitis PCR panel were negative for a wide range of viral, bacterial, and fungal targets, including herpesviruses, enterovirus, mumps virus, varicella-zoster virus, Escherichia coli K1, Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis, Streptococcus agalactiae, and Cryptococcus neoformans. HIV serology, cryptococcal antigen testing, and Toxoplasma gondii PCR were also negative.
Brain imaging added little at first glance. Cranial computed tomography was normal. Magnetic resonance imaging, however, showed bilateral white matter hyperintensities on T2-weighted, FLAIR, and diffusion-weighted sequences. Similar patterns have been described in meningitis caused by other pathogens, including cytomegalovirus and pneumococcus, so the imaging narrowed the field only modestly. The patient’s illness remained microbiologically unexplained until molecular testing was pursued beyond the standard panel.
Molecular Testing Identified the Pathogen
Empiric therapy began with intravenous ceftriaxone, ampicillin, dexamethasone, and acyclovir. Acyclovir was stopped once HSV-1 and HSV-2 CSF PCR results were negative. The case then moved into targeted diagnostic territory: CSF was tested by quantitative real-time PCR for parvovirus B19, Brucella spp., Leptospira spp., and C. psittaci, while serum underwent serologic testing for Coxiella burnetii, Brucella spp., Leptospira spp., and C. psittaci at Chile’s national reference laboratory.
The CSF PCR was positive for C. psittaci. Serology supported the diagnosis with an IgG titer of 1:128 and an IgM titer of 1:10, both meeting the positive cutoffs used in the investigation. The patient stayed clinically stable and never developed neurologic deficits. Repeat MRI on August 26, 2023, showed no pathologic findings. He completed 7 days of intravenous antibiotics followed by 7 days of oral levofloxacin and recovered fully as an outpatient.
The biological plausibility here is straightforward. C. psittaci is an obligate intracellular bacterium, and intracellular pathogens can evade routine culture-based detection while still provoking intense inflammatory responses in the CSF. When the usual panel is unrevealing, molecular assays become the most direct route to diagnosis.
Why This Case Widens the Differential for Atypical Meningitis
Human psittacosis has been documented previously in Chile, including a confirmed case in 1956, a family cluster in 1984, and a 15-case outbreak in 2021 in southern regions. None of those reports involved CNS disease. This case extends the geographic and clinical recognition of C. psittaci meningitis in Latin America.
A PRISMA 2020–guided systematic review placed the rarity in sharper focus. Only 6 previously published cases of molecularly confirmed C. psittaci CNS infection were identified worldwide: 1 from the United States, 4 from China, and 1 from Austria. The review excluded historical cases diagnosed only by serology or clinical judgment, leaving a small set of comparators in which molecular detection in CSF or CNS tissue anchored the diagnosis. Reported presentations ranged from isolated meningitis to severe encephalitis with status epilepticus or cerebral vasculitis.
One sentence captures the practical implication: rare zoonoses can masquerade as routine meningitis until molecular testing is ordered.
Diagnostic Strategy Depends on Exposure History and Early Specimen Collection
Routine bacterial culture cannot detect C. psittaci. Serology is more widely available, but paired samples are often needed and cross-reactivity with other Chlamydia species can blur interpretation. PCR performed early in illness offers the highest sensitivity and specificity, especially when the clinical picture is nonspecific and the CSF panel is negative.
Metagenomic sequencing may eventually broaden detection of unusual CNS pathogens, but access remains limited in many settings. In this patient, the key clue was not a dramatic neurologic exam or a pathognomonic scan. It was the combination of agricultural exposure, persistent febrile illness, inflammatory CSF, and the willingness to test beyond the standard menu.
The case also supports the treatment approach used here. Early empiric broad-spectrum coverage was followed by targeted therapy, and the patient recovered without deficit. Doxycycline remains the preferred antimicrobial for psittacosis, and a 21-day course is preferred when the CNS is involved, making timely recognition clinically important even when the initial presentation appears mild.
For rural and agricultural populations in Latin America, the unanswered diagnostic failure is often not the absence of disease but the absence of the right test.