CUTANEOUS AND SYSTEMIC PATHOLOGIC RESPONSES OF THE WEST AFRICAN DWARF GOAT TO SARCOPTES SCABIEI INFESTATION

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CUTANEOUS AND SYSTEMIC PATHOLOGIC RESPONSES OF THE WEST AFRICAN DWARF GOAT TO SARCOPTES SCABIEI INFESTATION

ABSTRACT

The pathophysiology of Sarcoptes scabiei infestation in the West African Dwarf goat was evaluated in a natural transmission study. Twenty- five adult male West African Dwarf (WAD) goats consisting of 15 naturally infested goats assigned into three equal groups based on severity of clinical disease as: A (mild infestation), B (moderate infestation), C (severe infestation), and10 healthy WAD goats with no previous history of mange infestation assigned into two equal groups as D (for contact transmission experiment) and uninfested control (E) were used for this study. Parameters assessed at the beginning of the study (week 0) and every two weeks thereafter included packed cell volume (PCV), haemoglobin concentration (Hb), erythrocyte count (EC), mean corpuscular volume (MCV), mean corpuscular haemoglobin (MCH), mean corpuscular haemoglobin concentration (MCHC), total leucocyte count (TLC), differential leucocyte count (DLC), total protein, serum albumin,  creatinine, adrenal and gonadal steroid hormones concentration (cortisol and testosterone), serum copper, zinc and vitamin A concentrations. At week 6 of the study, goats in the five groups were sacrificed and the testicular and epididymal sperm reserves were determined. Tissue sections of the infested skin of goats from groups A, B, C, D, and the normal control E were processed for histopathological studies. Data generated were analyzed using one-way analysis of variance (ANOVA), and variant means were separated using the Duncan’s multiple range test. Significance was accepted at p < 0.05.

There was wide variation in the susceptibility and severity of infestation in the group D goats (in-contact) as only three out of the five goats showed clinical signs of disease by the 6th week while mite was only demonstrated in two out of five by the 6th week. Lesions were anterio-posterior in distribution. There were significant (p < 0.05) reductions in PCV, Hb and EC mean values of the goats naturally infested with Sarcoptes scabiei in groups A, B and C relative to uninfested control group E at weeks 0, 2 and 4, but at week 6 all the infested groups including in-contact group D had a significantly (p < 0.05) lower PCV, Hb and EC compared to the control group E. There were no significant (p > 0.05) differences in some erythrocytic indices (MCV, MCH, MCHC) among the five groups of WAD goats. However, there was a significant (p < 0.05) increase in mean TLC in   groups B and C compared to groups A, D and the control, E. The increase in TLC was accompanied by a significant (p < 0.05) increase in both the absolute neutrophil and lymphocyte counts in groups B and C compared to groups A and E.  Significant (p < 0.05) difference in the mean monocyte count was only observed among the groups at week 6 in the group C compared to A, B, D and E. There was a  significant (p < 0.05) increase in mean eosinophil count in groups A and B compared to groups C, D and E throughout the period of study. Serum biochemical assay showed significant (p < 0.05) reduction in mean total protein in severely infested group C compared to groups A, B, D and E. There was no significant (p > 0.05) variation in mean serum albumin, globulin and creatinine levels among the groups throughout the period of study. The serum copper concentration was significantly (p < 0.05) lower in the naturally infested groups A, B and C when compared to in-contact group D and control group E. There were no significant (p > 0.05) differences in the  serum vitamin A and zinc levels between the groups although their levels were lower in naturally infested groups A, B, and C when compared to groups D and E. Although serum cortisol and testosterone concentrations were lower in the naturally infested groups A, B and C when compared to the in-contact group D and control group E, the differences were not statistically significant (p > 0.05). The mean testicular and epididymal sperm reserves decreased significantly (p < 0.05)  in all the Sarcoptes scabiei-infested groups A, B, C and D when compared to the control group E. Skin section of infested goats showed variable degrees of acanthosis, hyperkeratosis, parakeratosis and intracorneal pustules while the dermis had variable degrees of cellular infiltrate (neutrophils, eosinophils, lymphocytes) and fibroblast proliferation.

This study has established that sarcoptic mange in WAD goat led to decreased red blood cell counts, haemoglobin, packed cell volume (anaemia) but increased total white blood cell counts, neutrophils and lymphocytes. Serum biochemistry also indicated decreased total serum protein, albumin, copper, zinc, and vitamin A levels but increased creatinine. The most striking feature of the disease in WAD goats was the decreased testosterone levels and spermatogenesis. Histopathologic investigations showed that sarcoptic mange was associated with non-specific skin reactions such as parakeratosis, hyperkeratosis, acanthosis but most importantly epidermal pustules with varying degrees of dermal/epidermal cellular infiltration (neutrophils, eosinophils, lymphocytes) and dermal fibrosis.

 

TABLE OF CONTENTS

Title page        –           –           –           –           –           –           –           –           i

Declaration      –           –           –           –           –           –           –           –           iii

Certification    –           –           –           –           –           –           –           –           iv

Dedication      –           –           –           –           –           –           –           –           v

Acknowledgement      –           –           –           –           –           –           –           vi

Abstract          –           –           –           –           –           –           –           –           vii

Table of contents        –           –           –           –           –           –           –           x

List of tables   –           –           –           –           –           –           –           –           xv

List of figures  –           –           –           –           –           –           –           –           xvii

 

CHAPTER ONE       INTRODUCTION     –           –           –           –           1

1.1       Introduction    –           –           –           –           –           –           –           1

1.2     Objectives of the study –           –           –           –           –           –           3

 

CHAPTER TWO: LITERATURE REVIEW          –           –           –           4

2.1The West African Dwarf Goats     –           –           –           –           –           4

2.2 Mange       –           –           –           –           –           –           –           –           5

2.3 Sarcoptic mange   –           –           –           –           –           –           –          5

2.4 Psoroptic,Chorioptic and Demodectic mange in goats     –     –          6

2.5 Etiology of sarcoptic mange         –           –           –           –           –           8

2.6 Morphology of Sarcoptes scabiei –           –           –           –           –           8

2.7 Hosts         –           –           –           –           –           –           –           –           10

2.8 Transmission of Sarcoptes scabiei           –           –           –           –           11

2.9 Life cycle and epidemiology of Sarcoptes scabiei           –           –           11

2.10 Pathogenesis       –           –           –           –           –           –           –           12

2.11 Clinical signs and features-         –            –           –            –            13

2.12 Host immune response    –           –           –           –           –           –           13

2.13 Pathology            –           –           –           –           –           –           –           15

2.14 Diagnostic techniques     –           –           –           –           –           –           15

2.14.1 Clinical diagnosis        –           –           –           –           –           –           15

2.14.2 Light microscopy         –           –           –           –           –           –           16

2.24.3 Therapeutic diagnosis-           –          –           –         –         –          17

2.14.4 Dermatoscopy       –      –           –           –           –           –           –           17

2.14.5 Antigen detection and PCR technique –           –           –           –           18

2.14.6 Intradermal skin test for scabies          –           –           –           –           18

2.14.7 Antibody detection      –           –           –           –           –           –           18

2.15 Therapeutic management of sarcoptic mange    –           –           –           18

2.16 Control and prevention   –           –           –           –           –           –           19

 

CHAPTER THREE: MATERIALS AND METHODS      –           –           20

3.1 Experimental animals and housing           –           –           –           –           20

3.2 Feeding     –           –           –           –           –           –           –           –           21

3.3 Experimental Design        –           –           –           –           –           –           21

3.4 Parasitological Examination         –           –           –           –           –           21

3.5 Source of mite for in- contact transmission          –           –           –           22

3.6 Clinical monitoring of in-contact transmission experiment         –           22

3.7 Sample Collection            –           –           –           –           –           –           22

3.8 Haematological studies    –           –           –           –           –           –           23

3.7.4 Packed cell volume        –           –           –           –           –           –           23

3.7.5 Hemoglobin concentration        –           –           –           –           –           23

3.7.6 Erythrocyte counts         –           –           –           –           –           –           23

3.7.7 Erythrocytic indices       –           –           –           –           –           –           24

3.7.7A Mean corpuscular volume       –           –           –           –           –           24

3.7.7B Mean corpuscular hemoglobin            –           –           –           –           24

3.7.7C Mean corpuscular hemoglobin concentration –           –           –           24

3.7.8 Total leucocyte count    –           –           –           –           –           –           25

3.7.9 Differential leucocyte counts     –           –           –           –           –           25

3.8 Determination of serum total protein       –           –           –           –           26

3.8.2 Procedure           –           –           –           –           –           –           –           26

3.9 Determination of serum albumin  –           –           –           –           –           27

3.9.2 Procedure           –           –           –           –           –           –           –           27

3.10  Determination of serum creatinine        –           –           –           –           27

3.10.2 Procedure         –           –           –           –           –           –           –           27

3.11 Determination of serum vitamin A         –           –           –           –           28

3.11.2 Procedure         –           –           –           –           –           –           –           28

3.12 Determination of serum zinc and copper            –           –           –           2

3.12.2 Procedure         –           –           –           –           –           –           –           29

3.13 Adrenal and gonadal steroid concentration        –           –           –           29

3.13A Determination of serum testosterone   –           –           –           –           29

3.13B Procedure         –           –           –           –           –           –           –           29

3.13C Determination of serum cortisol          –           –           –           –           30

3.13D Procedure         –           –           –           –           –           –           –           30

3.14 Determination of gonadal and extra-gonadal sperm reserves    –           31

3.14.2 Procedure         –           –           –           –           –           –           –           31

3.14.2A Epididymal sperm reserve    –           –           –           –           –           31

3.14.2B Testicular sperm reserve       –           –           –           –           –           31

3.15 Histopathology   –           –           –           –           –           –           –           32

3.15.2 Procedure         –           –           –           –           –           –           –           32

3.16 Data Analysis      –           –           –           –           –           –           –           32

CHAPTER FOUR: RESULTS         –           –           –           –           –           33

4.1 Parasitological examinations        –           –           –           –           –           33

4.2 Clinical evaluation of experimentally exposed goats       –           –           35

4.3 Haematology         –           –           –           –           –           –           –           40

4.3.1 Packed cell volume        –           –           –           –           –           –           40

4.3.2 Haemoglobin concentraton        –           –           –           –           –           41

4.3.3 Erythrocyte count          –           –           –           –           –           –           42

4.3.4 Erythrocytic indices       –           –           –           –           –           –           43

4.3.4A Mean corpuscular volume       –           –           –           –           –           43

4.3.4B Mean corpuscular hemoglobin            –           –           –           –           44

4.3.4C Mean corpuscular hemoglobin concentration –           –           –           45

4.3.5 Total leucocyte count    –           –           –           –           –           –           46

4.3.6 Differential leucocyte counts     –           –           –           –           –           47

4.3.6A Absolute neutrophil count      –           –           –           –           –           47

4.3.6B Absolute lymphocyte counts   –           –           –           –           –           48

4.3.6C Absolute monocyte counts      –           –           –           –           –           49

4.3.6D Absolute eosinophil counts     –           –           –           –           –           50

4.3.6E Absolute basophil counts        –           –           –           –           –           51

4.4    Gonadal and extragonadal sperm reserve          –           –           –           52

4.4.1 Caput epididymal sperm reserve           –           –           –           –           52

4.4.2 Corpus epididymal sperm reserve          –           –           –           –           53

4.4.3 Cauda  epididymal sperm reserve          –           –           –           –           54

4.4.4 Total epididymal sperm reserve –           –           –           –           –           55

4.4.5 Right testicular sperm reserve   –           –           –           –           –           56

4.4.6 Left testicular sperm reserve      –           –           –           –           –           57

4.4.7 Combined testicular sperm reserve       –           –           –           –           58

4.5       Serum biochemical assay        –           –           –           –           –           59

4.5.1 Serum vitamin A, zinc and copper concentrations        –           –           60

4.5.2 Gonadal and Adrenal steroid concentrations     –           –           –           61

4.6 Histopathology     –           –           –           –           –           –           –           62

CHAPTER FIVE: DISCUSSION AND CONCLUSION   –           –           71

5.1 Discussions           –           –           –           –           –           –           –           71

5.2 Conclusions           –           –           –           –           –           –           –           75

REFERENCES          –                       –                    –                –      –      76

 

CHAPTER ONE

INTRODUCTION

1.1       Introduction

The rapid changing pattern of demand for livestock and livestock products emphasizes the importance of the livestock subsector to the agricultural economy of Nigeria.  Within the small ruminant husbandry, goat rearing plays an important role in the socio-economic life of the rural people in a developing country like Nigeria.  In southern Nigeria, the West African Dwarf goat is the most predominant small ruminant reared and over 70% of the rural community keeps them (ILCA, 1987; Olubunmi, 1995).  They are often termed the “poor man’s cow’’. Their small size permit them to be maintained on a limited area and they consume a wide variety of grasses, weeds, shrubs, tree leaves and crop residues that otherwise go waste and cause pollution (Kumar et al., 2010). Goat meat (Chevon) is preferred over other meats because it is leaner and suffers no religious taboos. Thus, in Nigeria, goats are kept for meat, as a source of cash income and manure among other socio-economic, religious and cultural reasons (Olubumni, 1995; Adeloye, 1998; Ujjwal and Dey, 2010).  In addition to the ability of the West African Dwarf goats to live and reproduce in harsh environmental conditions kidding twins and triplets, they are also valued as insurance or investment against crop failure (Devendra, 1976, Adeloye, 1998; ILRI, 1999; Jajasuriya, 1999; Minjauw and McLeod, 2003).

Disease problems in the small ruminants remains the major hurdle to the realization of the full potential of goat production for better economic return and research in the livestock industry, which need timely and effective intervention in management. (Francis, 1988; Kumar, et al., 2010). Infectious and non-infectious diseases influence the economic production of goats. Endo- and ectoparasitic diseases constitute a very important problem. From within the ectoparasites, the mite Sarcoptes scabiei imposes major economic and health threat to the production of West African Dwarf goats in southern Nigeria (Francis, 1988; Olubunmi, 1995; Okewole, 1997; Shoyinka et al., 2009).  The infestation by this mite popularly called sarcoptic mange, scabies or sarcoptidosis is a parasitic skin disease that has been described in more than 100 species of mammals including man (Ibrahim and Abu-Samra, 1987; Scott, 1988; Bornstein et al., 2001).It is known to be the most common, stubborn, unpleasant and difficult to treat of all mange infestations in the goat and there is now documented reports of its resistance to commonly known therapeutic drugs such as the avermectins (Jackson et al., 1983; Manurung et al., 1990; Smith and Sherman, 1994; Okewole, 1997; Currie et al., 2004; Shoyinka et al., 2009). The disease is characterized by intense pruritus, dermatitis, alopecia, emaciation, weakness, anorexia, very high morbidity and mortality in domestic and farm animals (Amsalu et al., 2000; Walton et al., 2004; Giadinis et al., 2011).  The mite inflicts severe damage to the hosts’ skin by forming tunnels within the upper epidermal layers (Morris and Dunstan, 1996) and transmission is believed to be by direct contact with infested domestic or wild animals, formites, pasture and flies (Kral and Schwartanan, 1964; Andrews, 1983; Jackson et al., 1983; Anderson et al., 2002; Curtis, 2004).  Although, epidemiological studies on Sarcoptic mange of goats in Nigeria reported prevalence rates of 17.27% and 15.66% in affected areas of southwestern and southeastern Nigeria respectively (Olubunmi, 1995; Shoyinka et al., 2009), mortality rates of 57% to 60% have been reported in some flock from different parts of the world (Amsalu et al., 2000; Nektarios et al., 2011).

Despite the economic and health importance of Sarcoptes scabiei infestation in both animal and human population, the pathogenicity, pathogenesis and pathology of the disease is poorly understood (Bornstein and Zakrisson 1993, Skerrat et al., 1999; Rambozzi et al., 2007). For instance, some studies reported that the lesions of Sarcoptes scabiei infestation are not limited to the skin alone and includes lymphoid hyperplasia, generalized lymphoadenopathy, hepatic and renal amyloidosis, hypothyroidism, bronchopneumonia as well as gonadal degeneration in both domestic and wild animals (Anderson, 1981; Folz, 1984; Arlian et al., 1990; Little et al., 1998; Skerrat et al., 1999; Nakagawa et al., 2009).

These extra dermal lesions are thought to be due to the adverse effects of pro-inflammatory cytokines or secretion of some toxins by mites that affects the vital organs.  However, the role of the highly reactive oxygen species (ROS) in the pathogenesis of ectoparasitic disease has become an area of hot debates in recent years, as excess free radical generation due to Sarcoptes scabiei infestation have been reported in goats and dogs (Camkerten et al., 2009; Ujjwal and Dey, 2010)  It is speculated that the combined effects of these free radicals and products of mite activity may be associated with organs dysfunction in scabies-infested animals (Ujjwal and Dey, 2010).

Available reports on the clinicopathology of sarcoptic mange in rabbits, dogs, foxes, sheep, camels, goats, pigs, coyotes and wild raccoon are inconsistent (Sheahan, 1975; Arlian et al., 1988a,1995; Dalapati et al., 1996;  Gorakh et al., 2000; Parmar et al., 2005; Hafeez et al., 2007; Shoyinka et al., 2009).  Such inconsistencies are most probably the result of host differences or severity of disease.

However, the tendency by previous workers to ignore the fact that the degree of severity is most likely to be directly related to the degree of systemic involvement in sarcoptic mange, adds to the difficulty of comparing the results of available and probably conflicting reports.  It is therefore necessary to have a better understanding of the pathophysiology of Sarcoptes scabiei infestations of goats using hematologic, biochemical and morphologic parameters based on the severity of clinical disease.

 

1.2     OBJECTIVES OF THE STUDY

1. To establish experimental contact transmission of sarcoptic mange to susceptible WAD goat.

2. To evaluate the effects of sarcoptic mange on the hematologic and some biochemical indices (including trace minerals and vitamin A) of WAD goat.

3. To assess the effects of sarcoptic mange on spermatogenesis (gonadal and extra-         gonadal sperm reserves), adrenal cortisol and gonadal hormone concentrationin WAD goat.

4. To document the histomorphologic changes in the skin sections of natural and experimental Sarcoptes scabiei-infested WAD goat.

 

 

 

CUTANEOUS AND SYSTEMIC PATHOLOGIC RESPONSES OF THE WEST AFRICAN DWARF GOAT TO SARCOPTES SCABIEI INFESTATION

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