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Table of Contents   
CASE REPORT  
Year : 2015  |  Volume : 8  |  Issue : 3  |  Page : 64-66
Toxoplasmosis in a 17-month-old Nigerian: A case report


1 Department of Pediatrics, Enugu State University Teaching Hospital, Enugu, Nigeria
2 Department of Pediatrics, University of Nigeria Teaching Hospital, Enugu, Nigeria

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Date of Web Publication25-May-2015
 

   Abstract 

Toxoplasmosis is the most serious manifestation of infection, resulting from the vertical transmission of Toxoplasma gondii (T. gondii) transplacentally, from a parasitemic mother to her offspring. It could also be acquired. Case Presentation: E.B is a 17-month-old female baby who presented with recurrent fever x 16/12., chronic cough x 16/12, recurrent stooling x 15/12, recurrent ear discharge x 15/12, failure to gain weight x 15/12, and delayed developmental milestones. Examination revealed an acutely ill- or chronically ill-looking child in mild respiratory distress, afebrile (36.5°C), anicteric, acyanozed, moderately pale, well hydrated with generalized lymphadenopathy (axillary, inguinal, cervical), no digital clubbing, and no pedal fullness. Computed tomography (CT) scan revealed bilateral basal ganglia calcifications with a focal cystic area in the left basal ganglia; bilateral multifocal intracerebral hypodensities were noted from the frontal to the occipital lobes at different levels bilaterally, with calcifications limited to the basal ganglia. Serological test revealed the patient's serum to be positive for toxoplasma immunoglobulin G (IgG). Conclusion: Toxoplasmosis, though rare, can cause mortality and morbidity in children. Thus, a high index of suspicion is warranted in management.

Keywords: Bilateral basal ganglia calcifications, immunoglobulin G (IgG), toxoplasmosis

How to cite this article:
Amadi OF, Ndu IK, Chinawa JM, Jean NC, Obidi NO. Toxoplasmosis in a 17-month-old Nigerian: A case report. Ann Trop Med Public Health 2015;8:64-6

How to cite this URL:
Amadi OF, Ndu IK, Chinawa JM, Jean NC, Obidi NO. Toxoplasmosis in a 17-month-old Nigerian: A case report. Ann Trop Med Public Health [serial online] 2015 [cited 2019 Nov 20];8:64-6. Available from: http://www.atmph.org/text.asp?2015/8/3/64/157632

   Introduction Top


Toxoplasmosis is a multispecies zoonotic disease caused by a parasite, Toxoplasma gondii (T. gondii). T. gondii is an obligate intracellular protozoan. [1] The fetus, newborn, and young infant with congenital toxoplasmosis are at risk of infection-associated complications, particularly retinal diseases that can occur in adulthood. Hosts, who are immunocompromised, are also at an increased risk for this severe disease. [3]

Toxoplasmosis is a common disease with worldwide distribution. The prevalence of congenital toxoplasmosis ranges from one case per 1,000 live births to one case per 10,000 live births. [4]

Following the feline ingestion of any of the forms of T. gondii, the parasite infects the gut epithelial cells and reproduces. The feline, then, excretes infectious oocysts in feces. [5]

Most infected infants appear healthy at birth. Often, they do not develop symptoms until months, years, or even decades later in life. [6]

Molecular diagnostic methods of diagnosing toxoplasmosis include techniques such as the conventional polymerase chain reaction (PCR). [7] PCR assay is capable of detecting T. gondii deoxyribonucleic acid (DNA). Detection of immunoglobulin G (IgG) is possible within 2 weeks of infection by performing the enzyme-linked immunosorbent assay (ELISA) test. [7]

Computed tomography (CT) scans may show multiple bilateral cerebral lesions while magnetic resonance imaging (MRI) has superior sensitivity (particularly if gadolinium is used for contrast) to CT scanning, and these often demonstrate single or multiple lesions, or more extensive diseases that are not apparent on CT scans. [7] Presently, the drugs used in the treatment of toxoplasmosis act primarily against the tachyzoite form of T. gondii; thus, they do not eradicate the encysted form (bradyzoite). [8] Pyrimethamine is the most effective agent and is included in most drug regimens.

This case is being reported because of its rarity and the need for a high index of suspicion in clinical practice. Early identification and appropriate intervention can significantly improve the quality of life.


   Case Report Top


E.B is a 17-month-old female baby who presented with recurrent fever x 16/12., chronic cough x 16/12, recurrent stooling x 15/12, recurrent ear discharge x 15/12, failure to gain weight x 15/12, and delayed developmental milestone.

Her mother had a febrile illness at a gestational age of 7 months, which was not associated with rash or jaundice. There was also a history of premature and prolonged rupture of membranes for about 2 days.

The patient was delivered at home through spontaneous vaginal delivery (SVD). The baby did not cry immediately after birth. Her birth weight was unknown; she had neither jaundice nor fever within 1 month of her life.

Examination revealed an acutely ill- or chronically ill-looking child in mild respiratory distress who was moderately pale with generalized lymphadenopathy. Her weight was 3 kg, which is 30% of the expected weight, and her head circumference was 38.5 cm (microcephaly).

Bilateral crepitations in the middle and the lower lung zones, hepatomegaly, and reduced muscle bulk in all the muscle areas with marked prominence of bony landmarks were observed. Her hair was hypopigmented, silky, and sparse, especially over the occipital and the temporal areas.

Ophthalmological assessment revealed normal eye anatomy. Examination of the fundus under the mydriasis showed features in keeping with bilateral chorioretinal degeneration.

Ear, nose, and throat (ENT) assessment revealed yellowish otorrhea seen in the right ear, while tympanic membrane (TM) was not seen. The left ear was clear and the TM was intact. Age-appropriate audiometric assessment was not done.

CT scan revealed bilateral basal ganglia calcifications with a focal cystic area in the left basal ganglia; bilateral multifocal intracerebral hypodensities are noted from the frontal to the occipital lobes at different levels bilaterally, with calcifications limited to the basal ganglia [Figure 1]. Serological test revealed that the patient was serum positive for toxoplasma IgG.
Figure 1: Brain CT-scan of the patient

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The mother's toxoplasma IgG, 57.2 IU/mL (0-10.5 IU/mL), was positive. Serum protein showed reversal of the albumin-globulin ratio. Liver functional test showed unconjugated hyperbilirubinemia, raised alanine transaminase, and aspartate transaminase.

Chest radiograph revealed accentuated right perihilar markings, some cystic consolidative changes in the lung fields, and left ventricular preponderance in spite of rotation with cerebrospinal fluid (CSF) pleocytosis.

Diagnosis of congenital toxoplasmosis was done and subsequently, the patient was commenced on pyrimethamine tablets with a dosage of 10 mg daily x 2/7, then 5 mg daily for 6/52, and clindamycin syrup with a dosage of 50 mg three times a day (tds) for 6/52.

She was also referred to the physiotherapist for expert management. At the time of discharge, her weight had increased to 55% of the expected weight; they are yet to come for follow-up visit.


   Discussion Top


This report revealed the existence of toxoplasmosis, though rare in our setting. Our index case is a 17-month-old female baby who presented with recurrent fever, chronic cough, ear discharge, and failure to gain weight. The clinical manifestations of toxoplasmosis vary greatly, producing a range of nonspecific symptoms. In immunocompetent patients, infection is usually asymptomatic or very mild. The common symptoms include fever, cervical lymphadenopathy, and other symptoms of generalized infection. The clinical course in immunocompromised patients can be much more severe, as noted in our patient. [9] This was corroborated by Cassius et al. [10] Ophthalmologic examination reveals multiple yellow-white cotton-like patches, with indistinct margins located in small clusters in the posterior pole showing chorioretinal degeneration. [9] This is akin to what was observed in our patient. There exists a female preponderance among children with toxoplasmosis, [10] and our index case is also a female. Cats, both wild and domestic, are the only definitive hosts for T. gondii. Eating raw eggs is also a predisposing factor. [10] Our patient was usually fed with raw eggs and her parents kept cats as pets. The delayed milestones seen in our patient can be explained by the intracerebral lesions, which can cause a static nonprogressive injury to a developing brain. This can result in several central nervous system (CNS) symptoms such as delayed milestones and delayed speech. [11]

CT scanning of the brain is useful in cerebral toxoplasmosis. Although multiple lesions are more common, finding a solitary lesion should not exclude toxoplasmosis. The lesions are characteristically hypodense and tend to occur at the corticomedullary junction; they frequently involve the basal ganglia. [12] Our index case also had lesions, which were basically located at the basal ganglia.

MRI scans often depict lesions or more extensive diseases that are not apparent on CT scans; however, we do not have this facility in our institution.

We obtained positive serum of toxoplasma IgG for the patient, but negative immunoglobulin M (IgM) and positive IgG from the maternal serum. However, it is known that the negative serology result does not exclude the diagnosis of toxoplasma infection in severely immunocompromised patients. [13]

Derouin et al. also noted the presence of IgG in the sera of 164 patients who had toxoplasmosis and who were immunocompromised. [13]

Our patient improved when she was put on a medication of pyrimethamine and clindamycin. The use of these drugs in the management of toxoplasmosis has been documented. [13]

 
   References Top

1.
Paquet C, Yudin MH; Society of Obstetricians and Gynaecologists of Canada. Toxoplasmosis in pregnancy: Prevention, screening, and treatment. J Obstet Gynaecol Can 2013;35:78-81.   Back to cited text no. 1
    
2.
Lindsay DS, Dubey JP. Toxoplasma gondii: The changing paradigm of congenital toxoplasmosis. Parasitology 2011;138:1829-31.   Back to cited text no. 2
    
3.
McLeod R, Boyer K, Karrison T, Kasza K, Swisher C, Roizen N, et al.; Toxoplasmosis Study Group. Outcome of treatment for congenital toxoplasmosis, 1981-2004: The National Collaborative Chicago-Based, Congenital Toxoplasmosis Study. Clin Infect Dis 2006;42:1383-94.   Back to cited text no. 3
    
4.
Alford CA Jr, Stagno S, Reynolds DW. Congenital toxoplasmosis: Clinical, laboratory, and therapeutic considerations, with special reference to subclinical disease. Bull N Y Acad Med 1974;50:160-81.  Back to cited text no. 4
[PUBMED]    
5.
Tenter AM, Heckeroth AR, Weiss LM. Toxoplasma gondii: From animals to humans. Int J Parasitol 2000;30:1217-58.  Back to cited text no. 5
    
6.
American Medical Association; American Nurses Association-American Nurses Foundation; Centers for Disease Control and Prevention; Center for Food Safety and Applied Nutrition, Food and Drug Administration; Food Safety and Inspection Service, US Department of Agriculture. Diagnosis and management of foodborne illnesses: A primer for physicians and other health care professionals. MMWR Recomm Rep 2004;53:1-33.  Back to cited text no. 6
    
7.
Tlamcani Z, Lemkhenete Z, Lmimouni BE. Toxoplasmosis: The value of molecular methods in diagnosis compared to conventional methods. J Microbiol Infect Dis 2013;3:93-9.   Back to cited text no. 7
    
8.
Sobrin L, Kump LI, Foster CS. Intravitreal clindamycin for toxoplasmic retinochoroiditis. Retina 2007;27:952-7.   Back to cited text no. 8
    
9.
Mandell GL, Bennett JE, Dolin R. Mandell, Douglas and Bennett′s Principles and Practice of Infectious Diseases. 6 th ed. Philadelphia: Elsevier, Churchill Livingstone; 2005. p. 3661.   Back to cited text no. 9
    
10.
Silva CS, Neves Ede S, Benchimol EI, Moraes DR. Postnatal acquired toxoplasmosis patients in an infectious diseases reference center. Braz J Infect Dis 2008;12:438-41.  Back to cited text no. 10
    
11.
Porter SB, Sande MA. Toxoplasmosis of the central nervous system in the acquired immunedefifiency syndrome. N Engl J Med 1992;327:1643-8.  Back to cited text no. 11
    
12.
Obtainable at Pediatric Toxoplasmosis Workup - Medscape Reference. Available from: http://emedicine.medscape.com/article/1000028-workup. [Last assessed on 2014 Sep 29].  Back to cited text no. 12
    
13.
Hellerbrand C, Goebel FD, Disko R. High predictive value of Toxoplasma gondii IgG antibody levels in HIV-infected patients for diagnosis of cerebral toxoplasmosis. Eur J Clin Microbiol Infect Dis 1996;15:869-72.  Back to cited text no. 13
    

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Correspondence Address:
Dr. Josephat M Chinawa
Department of Pediatrics, University of Nigeria Teaching Hospital (UNTH), PMB 01129, Enugu - 400 001, Enugu State
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.157632

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