1
1. Endocranial lesions in the left parietal (internal view) 2. Porotic lesions in the pars basilaris (inferior view) 3. Porotic lesions in the greater wings of the sphenoid (inferior view) 4. Porotic lesions in the mandible fragment (lateral view) 5. Porotic lesions in the right scapulae (anterior view) 6. Cribra humeralis in the right humerus (posterior view) Design: Ana Eduarda Sereijo (Sensebloom/ Grupo Dryas Octopetala) Joana Paredes 1 , Maria Teresa Ferreira 2 , Sofia N. Wasterlain 3 1 Department of Life Sciences, University of Coimbra/ iDryas, Grupo Dryas Octopetala, [email protected] 2 Styx, Grupo Dryas Octopetala / Forensic Sciences Centre, Portugal, [email protected] 3 Centro de Investigação em Antropologia e Saúde, Department of Life Sciences, University of Coimbra, [email protected] A Possible Case of Meningitis in a Modern Child from the wheel of Santa Casa da Misericórdia (Faro, Portugal) Early Illness: Introduction During growth, individuals are exposed to several environmental stress factors (1). These are generally divided in two groups: infection and malnourishment (2; 3). However, since it is not always possible to isolate the primary cause of growth retardation in a given population, epidemiological studies will depend largely on indirect evidences (2), known as non-specific stress indicators (3). These are usually chosen for their rather high rates of occurrence in skeletal samples, e.g. enamel hypoplasia, cribra orbitalia, porotic hyperostosis, non-specific periostitis and, more recently, endocranial lesions (1). Careful evaluation of the lesions’ morphology and distribution helps favouring one diagnosis at the expense of others. The aim of the present study is to make the differential diagnosis of an uncommon pathological case, recovered from an archaeological intervention in Santa Casa da Misericórdia (Faro, Portugal). The excavation brought to light the Santa Casa’s cemetery (16 th -19 th centuries) with several phases of funerary use, one of them with 51 non-adult inhumations (aged from foetus to one adolescent, most being less than 12 months), corresponding to abandoned new-borns received in the institution by foundling wheel’s mechanism means (5). Material and Methodology All bones of a well-preserved 2-year-old skeleton (age-at-death estimated by dental calcification) were examined under standardized lighting conditions by careful visual inspection, with the aid of a stereomicroscope. Results Discussion Several pathological conditions were considered as possible causes: Anaemia: Skeletal changes associated as part of a generalised syndrome called porotic hyperostosis, characterized by porous lesions of the ectocrania (mainly on the frontal, parietal and occipital bones). When the pitting is located on the superior wall of the orbit, it is known as cribra orbitalia (4; 7). Surface porosity results from marrow hyperplasia (4). The case: Cranial lesions’ morphology and distribution do not correspond to the typical features of anaemia. Also, the absence of cribra orbitalia does not favour such diagnosis. Scurvy: The most frequent and characteristic changes in the growing skeleton are due to haemorrhage (4; 8), which may stimulate the periosteum to produce new bone. This results in locally increased bone porosity to provide pathways for blood vessels (4; 7; 8). The most common locations are the external surface of the skull vault, the orbital walls, the sphenoid (4), the maxilla, the hard palate, the scapulae, and the metaphysis of long bones (4). Cranial marks consist in the development of small pores or in the deposition of new bone upon an underlying normal cortical (4). The case: The location of porotic lesions is consistent with scurvy, but the morphology of the cranial marks and the absence of reaction of the periosteum turn such condition unlikely. Rickets: Bone changes consist of inadequate mineralization of newly deposited bone during growth (9), due to vitamin D deficiency (4; 7), leading to bone porosity and roughening, especially next to the growth plates (9). Mechanical forces acting upon a weakened skeleton lead to multiple bone deformities, including spreading and concavity of metaphyses and diaphysial bending of long bones (4; 7). Cranial bone surfaces may be spicular, since superficial pores are relatively larger and represent voids as a result of imperfect mineralization of a growing surface rather than transmitting blood vessels (4). The case: Apart from the porosity displayed by some skull bones, a few diaphyses, and both scapulae, there are no deformities in the postcranial elements that could be related to rickets. Meningitis: It is an acute inflammation of the meninges, the membranes covering the brain (cerebral), the spinal cord (spinal) or both (7; 11), associated with several causes, being bacterial meningitis and tuberculous (TB) meningitis (10) two of the main forms. In areas of the skull vault affected by a relatively large focus of meningeal inflammation, characteristic impressions of atypical blood vessels can occur (10). Vestiges of TB meningitis are characterized not only by the changes described above, but also by relatively small, granular impressions whose diameter varies between 0.5 and 1.0 mm, which may be filled with lamellar bone at the bottom. These impressions, generally grouped in clusters, are situated at the endocranial face of the base, sometimes also at the lateral wall of the skull and at the cerebral fossa of the occipital bone (10; 11). They are caused by pressure atrophy of the tuberculars (10). The case: The observed cranial lesions match the ones produced by meningitis. The absence of small granulomata and arachnoid granulation favours the bacterial variant hypothesis at the expense of the tuberculous one (6). Postcranial evidences in the skeleton support this diagnosis, presenting themselves as signs of infection. Conclusions Differential diagnosis of the endocranial lesions present on a 2-year-old child led to the consideration of bacterial meningitis as the possible cause. The existence of several woven and porosity signs throughout the rest of the skeleton matches an infectious condition. Bearing in mind the environment where the foundling wheel’s children lived – orphanages with poor nutritional and hygienic conditions, exposure to pathogens was highly likely to occur. Besides, immature individuals wouldn’t be efficiently protected by their immune system. These circumstances could explain a case of meningitis. References 1. Lewis, M.; Roberts, C. 1997. Growing Pains: The Interpretation of Stress Indicators. International Journal of Osteoarchaeology, 7: 581-586. 2. Briend, A. 1998. Infection. In: Ulijaszek, S. J.; Johnston, F. E.; Preece, M. A. (eds) The Cambridge Encyclopaedia of Human Growth and Development. Cambridge, Cambridge University Press: 334–346. 3. Pinhasi, R. 2008. Growth in Archaeological Populations. In: Pinhasi, R.; Mays, S. (eds.) Advances in Human Palaeopathology. New York, Wiley-Liss: 363-380. 4. Mays, S. 2008. Metabolic Bone Disease. In: Pinhasi, R.; Mays, S. (eds.) Advances in Human Palaeopathology. New York, Wiley-Liss: 215-251. 5. Corga, M.; Ferreira, M. T. 2010. A acção caritativa da Santa Casa da Misericórdia de Faro: História e Bioarqueologia da 7ª obra corporal. Xelb, 10: 515-529. 6. Neves, M. J.; Corga, M.; Gonçalves, F.; Ferreira, M. T. 2010. Sondagens e Acompanhamento Arqueológico no edifício da Santa Casa da Misericórdia de Faro (Sé, Faro, Faro). Relatório Final. 7. Roberts, C.; Manchester, K. 2005. The Archaeology of Disease. New York, Sutton Publishing Limited. 8. Ortner, D.; Ericksen, M. 1997. Bone Changes in the Human Skull Probably Resulting from Scurvy in Infancy and Childhood. International Journal of Osteoarchaeology, 7: 212-220. 9. Mays, S.; Brickley, M.; Ives, R. 2006. Skeletal Manifestations of Rickets in Infants and Young Children in a Historic Population From England. American Journal of Physical Anthropology, 129: 362-374. 10. Roberts, C.; Buikstra, J. 2003. The Bioarchaeology of Tuberculosis. Gainesville, University Press of Florida. 11. Schultz, M. 2001. Paleohistopathology of Bone: A New Approach to the Study of Ancient Diseases. Yearbook of Physical Anthropology, 44: 106-147. Porotic Lesions Endocranial lesions + Porotic Lesions Porotic Lesions + Cribra 1 2 3 4 5 6 1 6 5 4 2 3

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Page 1: Early Illness - UC

1. Endocranial lesions in the left parietal (internal view)

2. Porotic lesions in the pars basilaris (inferior view)

3. Porotic lesions in the greater wings of the sphenoid (inferior view)

4. Porotic lesions in the mandible fragment (lateral view)

5. Porotic lesions in the right scapulae (anterior view)

6. Cribra humeralis in the right humerus (posterior view)

Design: Ana Eduarda Sereijo (Sensebloom/ Grupo Dryas Octopetala)

Joana Paredes1, Maria Teresa Ferreira2, Sofia N. Wasterlain3

1 Department of Life Sciences, University of Coimbra/ iDryas, Grupo Dryas Octopetala, [email protected] Styx, Grupo Dryas Octopetala / Forensic Sciences Centre, Portugal, [email protected]

3 Centro de Investigação em Antropologia e Saúde, Department of Life Sciences, University of Coimbra, [email protected]

A Possible Case of Meningitis in a Modern Child from the wheelof Santa Casa da Misericórdia (Faro, Portugal)

Early Illness:

Introduction

During growth, individuals are exposed to several environmental stress factors (1). These are generally divided in two groups: infection and malnourishment (2; 3). However, since it is not always possible to isolate the primary cause of growth retardation in a given population, epidemiological studies will depend largely on indirect evidences (2), known as non-specific stress indicators (3). These are usually chosen for their rather high rates of occurrence in skeletal samples, e.g. enamel hypoplasia, cribra orbitalia, porotic hyperostosis, non-specific periostitis and, more recently, endocranial lesions (1). Careful evaluation of the lesions’ morphology and distribution helps favouring one diagnosis at the expense of others.

The aim of the present study is to make the differential diagnosis of an uncommon pathological case, recovered from an archaeological intervention in Santa Casa da Misericórdia (Faro, Portugal). The excavation brought to light the Santa Casa’s cemetery (16th-19th centuries) with several phases of funerary use, one of them with 51 non-adult inhumations (aged from foetus to one adolescent, most being less than 12 months), corresponding to abandoned new-borns received in the institution by foundling wheel’s mechanism means (5).

Material and Methodology

All bones of a well-preserved 2-year-old skeleton (age-at-death estimated by dental calcification) were examined under standardized lighting conditions by careful visual inspection, with the aid of a stereomicroscope.

Results

Discussion

Several pathological conditions were considered as possible causes:

Anaemia: Skeletal changes associated as part of a generalised syndrome called porotic hyperostosis, characterized by porous lesions of the ectocrania (mainly on the frontal, parietal and occipital bones). When the pitting is located on the superior wall of the orbit, it is known as cribra orbitalia (4; 7). Surface porosity results from marrow hyperplasia (4).

The case: Cranial lesions’ morphology and distribution do not correspond to the typical features of anaemia. Also, the absence of cribra orbitalia does not favour such diagnosis.

Scurvy: The most frequent and characteristic changes in the growing skeleton are due to haemorrhage (4; 8), which may stimulate the periosteum to produce new bone. This results in locally increased bone porosity to provide pathways for blood vessels (4; 7; 8). The most common locations are the external surface of the skull vault, the orbital walls, the sphenoid (4), the maxilla, the hard palate, the scapulae, and the metaphysis of long bones (4). Cranial marks consist in the development of small pores or in the deposition of new bone upon an underlying normal cortical (4).

The case: The location of porotic lesions is consistent with scurvy, but the morphology of the cranial marks and the absence of reaction of the periosteum turn such condition unlikely.

Rickets: Bone changes consist of inadequate mineralization of newly deposited bone during growth (9), due to vitamin D deficiency (4; 7), leading to bone porosity and roughening, especially next to the growth plates (9). Mechanical forces acting upon a weakened skeleton lead to multiple bone deformities, including spreading and concavity of metaphyses and diaphysial bending of long bones (4; 7). Cranial bone surfaces may be spicular, since superficial pores are relatively larger and represent voids as a result of imperfect mineralization of a growing surface rather than transmitting blood vessels (4).

The case: Apart from the porosity displayed by some skull bones, a few diaphyses, and both scapulae, there are no deformities in the postcranial elements that could be related to rickets.

Meningitis: It is an acute inflammation of the meninges, the membranes covering the brain (cerebral), the spinal cord (spinal) or both (7; 11), associated with several causes, being bacterial meningitis and tuberculous (TB) meningitis (10) two of the main forms. In areas of the skull vault affected by a relatively large focus of meningeal inflammation, characteristic impressions of atypical blood vessels can occur (10). Vestiges of TB meningitis are characterized not only by the changes described above, but also by relatively small, granular impressions whose diameter varies between 0.5 and 1.0 mm, which may be filled with lamellar bone at the bottom. These impressions, generally grouped in clusters, are situated at the endocranial face of the base, sometimes also at the lateral wall of the skull and at the cerebral fossa of the occipital bone (10; 11). They are caused by pressure atrophy of the tuberculars (10).

The case: The observed cranial lesions match the ones produced by meningitis. The absence of small granulomata and arachnoid granulation favours the bacterial variant hypothesis at the expense of the tuberculous one (6). Postcranial evidences in the skeleton support this diagnosis, presenting themselves as signs of infection.

Conclusions

Differential diagnosis of the endocranial lesions present on a 2-year-old child led to the consideration of bacterial meningitis as the possible cause. The existence of several woven and porosity signs throughout the rest of the skeleton matches an infectious condition. Bearing in mind the environment where the foundling wheel’s children lived – orphanages with poor nutritional and hygienic conditions, exposure to pathogens was highly likely to occur. Besides, immature individuals wouldn’t be efficiently protected by their immune system. These circumstances could explain a case of meningitis.

References

1. Lewis, M.; Roberts, C. 1997. Growing Pains: The Interpretation of Stress Indicators. International Journal of Osteoarchaeology, 7: 581-586.

2. Briend, A. 1998. Infection. In: Ulijaszek, S. J.; Johnston, F. E.; Preece, M. A. (eds) The Cambridge Encyclopaedia of Human Growth and Development. Cambridge, Cambridge University Press: 334–346.

3. Pinhasi, R. 2008. Growth in Archaeological Populations. In: Pinhasi, R.; Mays, S. (eds.) Advances in Human Palaeopathology. New York, Wiley-Liss: 363-380.

4. Mays, S. 2008. Metabolic Bone Disease. In: Pinhasi, R.; Mays, S. (eds.) Advances in Human Palaeopathology. New York, Wiley-Liss: 215-251.

5. Corga, M.; Ferreira, M. T. 2010. A acção caritativa da Santa Casa da Misericórdia de Faro: História e Bioarqueologia da 7ª obra corporal. Xelb, 10: 515-529.

6. Neves, M. J.; Corga, M.; Gonçalves, F.; Ferreira, M. T. 2010. Sondagens e Acompanhamento Arqueológico no edifício da Santa Casa da Misericórdia de Faro (Sé, Faro, Faro). Relatório Final.

7. Roberts, C.; Manchester, K. 2005. The Archaeology of Disease. New York, Sutton Publishing Limited.

8. Ortner, D.; Ericksen, M. 1997. Bone Changes in the Human Skull Probably Resulting from Scurvy in Infancy and Childhood. International Journal of Osteoarchaeology, 7: 212-220.

9. Mays, S.; Brickley, M.; Ives, R. 2006. Skeletal Manifestations of Rickets in Infants and Young Children in a Historic Population From England. American Journal of Physical Anthropology, 129: 362-374.

10. Roberts, C.; Buikstra, J. 2003. The Bioarchaeology of Tuberculosis. Gainesville, University Press of Florida.

11. Schultz, M. 2001. Paleohistopathology of Bone: A New Approach to the Study of Ancient Diseases. Yearbook of Physical Anthropology, 44: 106-147.

Porotic Lesions

Endocranial lesions + Porotic Lesions

Porotic Lesions + Cribra

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1

6

5

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2

3